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BACKGROUND: During intervertebral disc degeneration, mitophagy plays an extremely important role in preventing the progression of intervertebral disc degeneration. Regulating the level of mitophagy may be a new strategy for the treatment of intervertebral disc degeneration. OBJECTIVE: To review the relationship between mitophagy and intervertebral disc, in order to provide a reference for the treatment of intervertebral disc degeneration by regulating the level of mitophagy. METHODS: A literature search was performed in CNKI, Wanfang, VIP, and PubMed using “intervertebral disc degeneration, mitophagy, targeted therapy, inflammation, signaling pathways” as Chinese and English search terms. Finally, 54 articles were included and summarized. RESULTS AND CONCLUSION: (1) At present, the specific mechanism of intervertebral disc degeneration is not clear. A large number of studies have shown that intervertebral disc degeneration is closely related to mitophagy, which involves a relatively complex mechanism and pathway. Among various pathways, PINK1/ Parkin is the most widely studied signaling pathway for mitophagy regulation. (2) Some drugs, such as Salidroside, Urolithin A, Honokiol, MitoQ, have been found to have the potential to treat intervertebral disc degeneration by regulating the level of mitophagy. These drugs have shown positive preclinical results. (3) At present, the targeted therapy of mitophagy is mainly preclinical research and has achieved positive results. Further clinical research is needed to explore its clinical efficacy and safety. [ABSTRACT FROM AUTHOR]

BACKGROUND: Berberine has the potential to induce osteogenic differentiation of various mesenchymal stem cells under normal conditions and special conditions such as high glucose, infection and inflammation. It is a natural small molecule drug that can induce bone formation in seed cells instead of growth factors, and has great application prospect in bone tissue engineering. OBJECTIVE: To review and summarize the research progress in the osteogenic mechanism and efficacy of berberine, especially its osteogenic potential under high glucose, infection and inflammation conditions, and its biological safety, so as to provide theoretical basis for its development and application in bone tissue engineering. METHODS: PubMed, WanFang, and CNKI were searched for relevant literature using the keywords of “berberine, bone defects, bone repair, bone regeneration, osteoinductive, osteoporosis, osteoblast, osteoclast, bone tissue engineering, bone, high glucose, diabetes, inflam*, infect*” in English and Chinese, respectively. A total of 105 literatures were selected for review. RESULTS AND CONCLUSION: Berberine can be used to treat multiple diseases including bone diseases, and it has the ability to promote bone regeneration. This article systematically reviews the mechanism of berberine on bone regeneration and in vivo and in vitro studies. Studies have shown that it can play a role in bone repair by promoting osteogenesis, inhibiting osteoclast formation and activity, and preventing osteoporosis. It shows excellent osteogenic differentiation potential mainly via Wnt/β-catenin, PI3K/AKT, EGFR/MEK/p38MAPK, cAMP/PKA/CREB, ERK and other signaling pathways. Berberine can also relieve the inhibition of osteogenic differentiation caused by high glucose, infection and inflammation, which provides more possibilities for the treatment of bone defects in patients with diabetes or infection and inflammation in the bone defect site. Berberine also has the advantages of low toxicity, low price, easy access (currently it can be synthesized), which is a relatively ideal bone induction potential drug. In recent years, the application of berberine in the treatment of bone defect tends to be localized, mainly through the combination with bone tissue engineering technology to improve bioavailability, and has shown good bone repair effect and excellent biological safety in animal experiments. In addition, preclinical experiments have shown splendid bone regeneration potential in the conditions of diabetes, local infection and inflammation. In the future, more studies are needed to fully reveal the osteogenic mechanism and biological safety of berberine, and seek the most suitable controlled release loading system to make artificial bone replacement materials with good mechanical strength, efficacy and biological safety. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the underlying mechanism of metformin's protective effect on articular cartilage in rats afflicted with osteoarthritis. Methods Thirty male SD rats were randomly divided into three groups (n = 10 per group) to establish a rat model of knee osteoarthritis. The metformin group received metformin via gavage [200 mg/kg·d)], while the control and model groups received saline as a control. After 4 weeks, morphological staining was used to observe articular cartilage morphology, and immunohistochemical staining, immunofluorescence staining, and Western blot were employed to detect the expression of factors related to the SIRT1/p53 signaling pathway, inflammation, and apoptosis. Results Compared to the model group, the metformin group exhibited significantly reduced cartilage structural damage, characterized by a smoother cartilage surface, increased chondrocyte population, and enhanced proteoglycan content. Immunohistochemical staining, immunofluorescence staining, and Western blot analysis revealed significantly higher expression levels of SOX9, Aggrecan, Bcl-2, and SIRT1 proteins in the metformin-treated cartilage tissue compared to the model group. Conversely, lower expression levels of IL-6 TNF-α BAX Caspase-9 and p53 proteins were observed in the metformin group compared to the model group. TUNEL staining results demonstrated a significant reduction in apoptotic chondrocytes within the metformin treated group when compared with the model group. Conclusion Metformin exerts a protective effect on articular cartilage in SD rat models of osteoarthritis by activating the SIRT1/p53 signaling pathway, leading to decreased chondrocyte apoptosis and inhibition of extracellular matrix degradation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Diabetic ulcers are a common complication of diabetes mellitus, which is manifested as foot ulcers complicated with infection, long treatment cycle, high disability rate and mortality rate, and brings a heavy burden to patients and social care. OBJECTIVE: To review the mechanism of action and the latest treatment progress of traditional Chinese medicine (TCM) in the treatment of diabetic ulcers, and to provide a basis for further theoretical research and clinical application. METHODS: CNKI, WanFang Database and PubMed database were searched for relevant literature using the keywords of “diabetic ulcer, medicinal herb, inflammation, interleukin-1β, interleukin-6, tumor necrosis factor, hypersensitive C-reactive protein, γ-interferon, interleukin-4, interleukin-10” in Chinese and English, respectively. The relevant literature in recent years was searched, and finally 75 articles were included for review. RESULTS AND CONCLUSION: The high glucose environment of the body will increase the level of pro-inflammatory cytokines, so that diabetic ulcer wounds are in a state of chronic inflammatory response for a long time, and difficult to heal or even not heal. TCM has summed up a lot of experience in the long-term struggle with diabetic ulcer. At present, TCM divides diabetic ulcers into four syndrome types: dampness and heat poison syndrome, blood and blood stasis obstruction pattern, heat poison injury Yin pattern, and Qi and blood deficiency syndrome, as well as representative prescriptions for treatment. According to their clinical characteristics, diabetic ulcers can be also divided into three stages: primary, middle and late stages. Different treatment methods are proposed: “clear method,” “warm and clear combined use” and “maintenance method.” Under the guidance of dialectical typing and staging of TCM, TCM monomers, extracts and compounds inhibit the inflammatory response and promote the healing of diabetic ulcers by down-regulating the expression of pro-inflammatory factors and/or up-regulating the expression of anti-inflammatory factors. Compared with modern medicine, TCM has significant advantages in the treatment of diabetic ulcers. There are many TCM monomers, extracts and compounds for the treatment of diabetic ulcers, such as angelica, curcumin, improved Chonghe ointment, Sanhuang blood exhaustion prescription and sore-ulcer I. formula, etc. It has been found that TCM for the treatment of diabetic ulcers is mainly heatclearing and detoxifying, invigorating blood circulation and removing blood stasis, and amassing sores and muscle-building drugs, and the frequency of use, treatment scope and therapeutic effect of TCM compounds are obviously better than those of TCM monomers and extracts. Among them, the most commonly used are the Sanhuang blood exhaustion prescription and the sore-ulcer I as well as prescription for the treatment of damp heat toxicity syndrome and Zizhu ointment for the treatment of non-ischemic diabetic ulcers. However, there are also some shortcomings in the treatment of diabetic ulcers with TCM. First, there are few clinical syndrome studies on diabetic ulcers. Secondly, there are a wide variety of TCM monomers, extracts and compounds for the treatment of diabetic ulcers, and the relevant research is insufficiently in-depth. Finally, the research on the mechanism underlying TCM treatment of diabetic ulcers is still in the preliminary exploration stage, and the mechanism of action still needs to be further explored. In the future, it is necessary to strengthen the research on the pharmacology of TCM and the clinical syndrome of diabetic ulcers, analyze the potential targets and related signaling pathways of TCM in the treatment of diabetic ulcers, give full play to the therapeutic advantages of TCM with multiple targets, multiple pathways, multiple levels and multiple systems, and develop TCM with significant efficacy, active ingredients and clear targets. [ABSTRACT FROM AUTHOR]

Objective To elucidate the key targets and the mechanism of Jiegeng Decoction in treating chronic pharyngitis through an integrated approach of network pharmacology and molecular docking, and to verify the predicted results through animal experiments. Methods A rat model of chronic pharyngitis was induced by β-hemolytic streptococcus to assess the impact of Jiegeng Decoction on serum inflammatory factors and the pathological alterations in pharyngeal tissues. Key targets associated with chronic pharyngitis were identified through databases such as OMIM, DrugBank, and GeneCards. The chemical constituents of Jiegeng Decoction were characterized by UHPLC-QE-MS coupled to the TCMSP and swisstarget Predicition databases. Subsequently, STRING database was applied to construct protein-protein interaction network of key targets, and the Database for Annotation, Visualization and Integrated Discovery (DAVID)was utilized to perform Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Furthermore, molecular docking of the active components with the core targets was performed by using AutoDock Tools1.5.6. Western Blot was carried out to verify prediction results. Results In vivo studies revealed that Jiegeng Decoction significantly decreased the serum levels of IL-1β, IL-6, TNFα, ICAM-1, and MCP-1 in rats with chronic pharyngitis (P＜0.05), and ameliorated the pathological damage in pharyngeal tissues. A total of 94 principal bioactive components were obtained, which acted synergistically on 311 targets, participated in responses to exogenous stimuli, drug metabolism, and protein tyrosine kinase activities, and played a significant regulatory role in the PI3K/AKT, MAPK, and Ras signaling pathways. The results of molecular docking showed that there was a strong binding ability between the key targets and the active ingredients. Western Blot analysis indicated that Jiegeng Decoction notably reduced the expression of the TLR4 protein and the phosphorylation level of P38 MAPK. Conclusion Jiegeng Decoction exerts its therapeutic effect on chronic pharyngitis by modulating the TLR4/P38 MAPK signaling pathway, attenuating serum inflammatory factors, and reversing the pathological changes in pharyngeal tissues. [ABSTRACT FROM AUTHOR]

Calcific aortic valve disease (CAVD) is a progressive heart valve disorder, which has similar pathogenesis of atherosclerosis, involving lipid deposition, inflammatory response, and extracellular matrix remodeling. Inflammation plays a crucial role in the pathogenesis of CAVD. Macrophages as central executors of the inflammatory response, whose polarization state is closely related to disease progression. Traditional Chinese medicine (TCM) theory suggests a close connection between macrophage polarization and yin-yang theory. This paper introduces the effect of macrophage with different polarization states on CAVD, as well as the role and mechanisms of TCM in regulating macrophage polarization to prevent and treat CAVD through muti-pathway, aiming to provide new insights for the treatment of CAVD with TCM. [ABSTRACT FROM AUTHOR]

Osteoporosis (OP) is a common systemic bone metabolic disease clinically, mainly induced by the imbalance or deviation of bone homeostasis caused by various factors. Abundant research has confirmed that long non-coding RNA (IncRNA), such as IncRNA XIST, plays a crucial role in the metabolic imbalance processes of OP, such as bone homeostasis imbalance or deviation, proliferation and apoptosis of chondrocytes, and interactions between miRNA and proteins. This may provide a new perspective for in-depth exploration of the pathogenesis of OP. This article aims to review the relevant studies of IncRNA XIST in OP, in order to reveal its key mechanisms in the occurrence and development of OP, and provide theoretical support for the clinical treatment of bone metabolic diseases using IncRNA XIST. [ABSTRACT FROM AUTHOR]

Objective To investigate the impacts of salidroside (Sal) on inflammatory injury of articular chondrocytes. Methods Experimental group: Human articular chondrocytes were separated into control group (conventional culture), IL-1β group (50 ng/ mL), Sal-2 µmol/L, Sal-4 µmol/L, Sal-8 µmol/L groups, and Sal+GW0742 group (8 µmol/L Sal+4 µmol/L CCL2-CCR2 signal axis activator GW0742). Human articular chondrocytes were treated with 50ng/mL IL-1β to establish the injury model of articular chondrocytes. MTT method was applied to detect the toxicity of Sal and GW0742 on articular chondrocytes. Plate cloning experiments and flow cytometry were applied to detect cell proliferation and apoptosis. ELISA was applied to detect the levels of inflammation related factors (IL-10, TNF-α, IL-6). QRT-PCR was applied to detect the expression of CCL2 and CCR2 mRNA in cells. Western blot was applied to detect the expression of proliferation and apoptosis related proteins (PCNA, Cleaved Caspase-3) and CCL2-CCR2 signaling axis proteins. Results Compared to the control group, the number of colony formation, the expression of IL-10, and PCNA reduced in the IL-1β group, the apoptosis rate, the expression of TNF-α, IL-6, CCL2, CCR2 mRNA, and the expression of Cleaved Caspase-3, CCL2, and CCR2 increased (P<0.05). Compared to the IL-1β group, the number of colony formation, the expression of IL-10, and PCNA in the Sal-2 µmol/L, Sal-4 µmol/L, and Sal-8 µmol/L groups increased sequentially, the apoptosis rate, the expression of TNF-α, IL-6, CCL2, CCR2 mRNA, and the expression of Cleaved Caspase-3, CCL2, and CCR2 decreased sequentially (P<0.05). CCL2-CCR2 signaling pathway activator GW0742 was able to weaken the protective effect of Sal on IL-1β-induced inflammatory injury of articular chondrocytes (P<0.05). Conclusion Sal may inhibit IL-1β-induced apoptosis and inflammatory response of articular chondrocytes by inhibiting the CCL2-CCR2 pathway. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Dermatovenereology is the property of Xi'an Jiaotong University Periodicals Center and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: For early knee osteoarthritis in which total knee arthroplasty fails to achieve satisfactory results, high tibial osteotomy that has been found to promote regeneration of damaged cartilage and alleviate symptoms in patients is considered a classic knee-preserving procedure. OBJECTIVE: To review and discuss the effectiveness, mechanism, and application prospects of high tibial osteotomy in stimulating cartilage regeneration in knee osteoarthritis and to provide a theoretical basis for the use of high tibial osteotomy in the treatment of knee osteoarthritis. METHODS: A computerized search was conducted in PubMed, Web of Science, CNKI and WanFang databases for relevant literature published from 2013 to 2023. The search terms used were “knee osteoarthritis, high tibial osteotomy, limb alignment, chondrocytes, biomechanics, intra-articular” in both English and Chinese. Finally, 75 articles were included for review. RESULTS AND CONCLUSION: High tibial osteotomy correcting the lower limb alignment has been found to be effective in alleviating symptoms and potentially delaying or preventing the need for total knee arthroplasty. This is an important aspect of orthopedic step-down treatment in knee osteoarthritis. Maintaining a normal mechanical microenvironment is crucial for the proper functioning and maintenance of chondrocyte phenotype. Abnormal mechanical signals can be converted into intracellular chemical signals through mechanosensors like primary cilia, integrins, cytoskeleton and nucleoskeleton, resulting in disruptions to the balance of matrix metabolism and regulation of inflammatory responses. Chondrocytes after abnormal stress action still have the potential to revert to a normal phenotype under appropriate stress; correction of the mechanical microenvironment by high tibial osteotomy leads to spontaneous cartilage repair and remission of synovial inflammation. The combination of high tibial osteotomy and cartilage regeneration strategy holds promising prospects for patients with early knee osteoarthritis who are not candidates for total knee arthroplasty. [ABSTRACT FROM AUTHOR]

BACKGROUND: Platelet-rich fibrin (PRF) is a second generation platelet concentrate with the advantages of simple operation, no anticoagulant, and high bioactivity, which has been applied in the fields of trauma repair, bone defect repair, and tendon soft tissue repair, and has been proved to have a certain tissue repair-promoting effect. OBJECTIVE: To study the repair effect of PRF on articular cartilage tissue in rats with knee osteoarthritis. METHODS: Thirty-six Sprague-Dawley rats were randomly divided into normal group, model group, and PRF group, with 12 rats in each group. Rats in the normal group did not undergo any treatment. In the model group, animal models of knee osteoarthritis were prepared and rat models were then given physiological saline into the joint cavity once a week after surgery. Rat models of knee osteoarthritis were also prepared in the PRF group, and autologous PRF was injected into the joint cavity once a week after surgery. After 5 weeks of continuous treatment, tissue samples were taken. Hematoxylin-eosin staining was used to observe the morphology of cartilage tissue. Tunel staining was used to detect chondrocyte apoptosis, ELISA was used to detect inflammatory factor levels. Western blot and RT-PCR were used to detect Bcl-2, Bax, and Caspase-3 expression in protein and mRNA levels, respectively. RESULTS AND CONCLUSION: The model group had severe cartilage tissue damage, while the PRF group had significantly improved cartilage tissue morphology compared with the model group. The model group had more apoptotic chondrocytes. Compared with the model group, the mean absorbance of Tunel positive staining in the PRF group significantly decreased (P < 0.01). The levels of interleukin-1β, interleukin-6 and tumor necrosis factor-α were significantly increased in the model group and PRF group compared with the normal group (P < 0.01) and were significantly decreased in the PRF group compared with the model group (P < 0.01). The relative expressions of Bax and Caspase-3 at protein and mRNA levels were significantly increased in the model group and PRF group compared with the normal group (P < 0.01), while the relative expressions of Bcl-2 at protein and mRNA were significantly decreased (P < 0.01). Compared with the model group, the relative expression of Bax and Caspase-3 at protein and mRNA levels were significantly decreased in the PRF group (P < 0.01), while the relative expressions of Bcl-2 at protein and mRNA levels were significantly increased (P < 0.01). To conclude, PRF can inhibit chondrocyte apoptosis by inhibiting the expression of pro-inflammatory factors, thereby promoting cartilage tissue repair in knee osteoarthritis rats. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) is a common and serious kidney disease with rising incidence and mortality rates. Disruption of fatty acid oxidation (FAO) is a significant pathological feature in the progression of AKI. Under AKI conditions, renal tubular epithelial cells (RTECs) undergo marked energy metabolic reprogramming, with particularly notable disturbances in fatty acid metabolism. Therefore, exploring the mechanisms associated with impaired fatty acid metabolism is crucial for developing effective therapies for AKI. This review comprehensively discusses the alterations in lipid metabolism in AKI, including fatty substances and metabolic enzymes related to FAO. It summarizes the adverse reactions caused by FAO metabolic reprogramming, such as autophagy, apoptosis, inflammation, and oxidative stress in cells. The review proposes that supplementing FAO-related metabolic products or inhibiting FAOrelated regulatory enzymes can effectively reverse abnormal metabolic processes in the kidneys, thereby reducing inflammation and oxidative stress, leading to effective treatment of AKI. This work provides insights that may facilitate further clinical research on AKI. [ABSTRACT FROM AUTHOR]

BACKGROUND: Mesenchymal stem cells possess characteristics such as rapid renewal, targeted homing, tissue repair, and immune regulation, which provide potential for the treatment of inflammatory diseases. In most inflammatory diseases, interleukin-1β is highly expressed. Both exogenous and endogenous mesenchymal stem cells unavoidably exist in an environment with high interleukin -1β concentration. OBJECTIVE: To study the interaction of interleukin-1β with mesenchymal stem cells in inflammatory environment and the mechanism of its influence on the migration and adhesion of mesenchymal stem cells to provide a theoretical basis for adjusting stem cell therapy strategies. METHODS: The first author searched for studies involving interleukin-1β enhancing migration and adhesion of mesenchymal stem cells by computer on CNKI, WanFang, VIP, PubMed, and Web of Science using search terms “interleukin-1β, mesenchymal stem cell, nuclear factor-κB, MAPK, ERK, p38, migration, adhesion” in Chinese and English. The literature tracing method was also used to search for some of the literature. Finally, 65 articles were included in the review analysis. RESULTS AND CONCLUSION: (1) In the inflammatory environment, interleukin-1β can regulate the migration and adhesion ability of mesenchymal stem cells. This effect may be achieved by recruiting IRAK1 through interleukin-1RI and then activating TAK1 and IKK in turn. After IKK phosphorylation, nuclear factor-κB and ERK signaling pathways are activated or CXCR expression is upregulated through the p38 pathway to promote mesenchymal stem cell migration and adhesion. However, further standardized research needs to be carried out based on the genetic background of mesenchymal stem cells, the dose and processing time of interleukin-1β. (2) In vitro experiments using pre-stimulated mesenchymal stem cells with interleukin-1β can change the survival environment of mesenchymal stem cells and alter their secretion factors to make them develop towards a more anti-inflammatory direction. On the other hand, under the premise of producing higher levels of anti-inflammatory and pro-nutrient factors, extracted mesenchymal stem cell exosomes can exert antiinflammatory effects. (3) It has been observed in various animal disease models that pre-stimulating mesenchymal stem cells with interleukin-1β regulates their immune regulation ability, thereby affecting the development and outcome of inflammation. However, this is limited to preclinical basic research only; further verification on efficacy and safety of stem cell therapy with interleukin-1β pre-treated mesenchymal stem cells is required in clinical settings. [ABSTRACT FROM AUTHOR]

BACKGROUND: Stem cell therapy has become an emerging method of treating pathological scars. miRNAs are involved in scarring mechanisms, and the targeted action of some stem cell sources of miRNA is mediated by exosomes. OBJECTIVE: To review the biological properties of miRNA derived from mesenchymal stem cells and its derivatives, the mechanism of treatment of scarring through anti-inflammation, suppression of excessive tissue reconstruction and antioxidation. METHODS: The first author used a computer in September 2023 to retrieve the relevant literature published from January 2000 to September 2023, searching for “stem cell, exosome, miRNA, keloid” in English, and “stem cells, exosome, keloid” in Chinese, eventually incorporating 74 papers for analysis. RESULTS AND CONCLUSION: (1) miRNAs with high expression of exosomes derived from mesenchymal stem cells increase the proportion of M2-type macrophages by promoting the polarization of macrophages, target the regulation of transforming growth factor β, transforming growth factor β receptors or related signaling pathways, inhibit the expression of pro-inflammatory factors, promote the expression of anti-inflammatory factors and other mechanisms to inhibit inflammation and thus suppress scar lesions. (2) miRNAs with high expression of exosomes derived from mesenchymal stem cells can reduce the secretion of matrix metalloproteinases, regulate the balance between matrix metalloproteinase inhibitors and matrix metalloproteinases, inhibit the proliferation and migration of fibroblasts and myofibroblasts, directly reduce the production of collagen and other mechanisms, and ultimately lead to the normal degradation of extracellular matrix, thereby inhibiting excessive tissue remodeling and cicatricial lesions. (3) miRNAs with high expression of exosomes from mesenchymal stem cells can improve the resistance of scar fibroblasts to oxidative stress by regulating reactive oxygen species and hypoxia-inducing factors, and then regulate the proliferation and apoptosis of scar fibroblasts to inhibit scar lesions. (4) Exosomes derived from mesenchymal stem cells have good prospects for scar treatment. Studies on this aspect can find mirnas that regulate inflammatory cells, inflammatory factors, signaling pathways, matrix metalloproteinases, fibroblasts, reactive oxygen species, hypoxia-inducing factors and other key factors from the three aspects of inflammation, tissue remodeling and oxidative stress. Then, by inducing mesenchymal stem cells with high expression of the above miRNA, exosomes were extracted, and finally verified and clinical trials were carried out. [ABSTRACT FROM AUTHOR]

Objective: To study the differences of gene expression and functional enrichment of peripheral blood leukocytes between pediatric patients with obstructive sleep apnea (OSA) and healthy children. Methods: 5 children diagnosed with OSA were selected as the case group and 7 healthy children were selected as the control group. Venous blood (3mL) was collected in the morning after polysomnography monitoring. White blood cells were isolated by centrifuge and then RNA was extracted for high-throughput sequencing and transcriptome analysis. Differentially expressed genes were identified, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment, as well as protein-protein interaction analysis. Results: There were significant differences in the gene expression levels of peripheral blood leukocytes between the case group and the control group, mainly in the biological processes related to inflammatory response and hypoxia. The signaling pathways involved include the interaction between cytokines and their receptors, Toll-like receptor signaling pathway and MAPK signaling pathway. Key interacting proteins involved include cell cycle regulatory proteins (e.g. CDK1, CCNB1, BUB1), interferon-inducing proteins (e.g. IFIT1, XAF1), and various cytokines (e.g. CXCL8, IL6, TNF). Conclusions: The expression of immune and inflammation-related genes in peripheral white blood cells of children is significantly changed, suggesting systemic inflammation, which may be a potential mechanism of OSA in children. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of Chronic intermittent hypoxia on the short-term memory and possible mecha- nisms involved. Methods: The 8 weeks male C57BL/6 mouse were randomly divided into Room Air (RA) and Chronic intermittent hypoxia (CIH) group. The CIH mice were exposed to CIH four weeks during the light phase (9 a.m.-9 p.m.). Measure the body weight of mice before and after the CIH; Open field test (OFT) and new object recognition tests (NORT) were used to assess autonomous motor ability and short-term memory of mice respond to CIH after four weeks, respectively. Hippocampus tissues were obtained to observe the neuron changes through Nissl Staining; Immunofluorescence staining and qRT-PCR were used to detect the activation of astrocytes in hippocampus tissue of mouse; Elisa detected changes in TNFα, IL-6, and IL-1β in mouse hippocampus tissue. Results: After 4 weeks of intermittent hypoxia, the average body weight of the RA group mice was significantly higher than that of the CIH group, and the difference was statistically significant (P=0.002); The results of the OFT showed that there was no significant difference in total exercise distance (P=0.3156) and velocity between the RA and CIH groups of mice (P=0.3157); There was no significant difference in the recognition index between the two groups of mice during the training period of the NORT test (P=0.1596). During the testing period of the NORT test, CIH mice spent less time exploring new objects than RA mice, and the recognition index of the CIH group was significantly lower than that of the RA group (P=0.0063); Nissl staining showed that neurons in the hippocampus CA1 of CIH mice were sparse and Nissl bodies were pale; Immunofluorescence staining showed that the relative GFAP positive area in the hippocampus CAl region of CIH mice was higher than that in the RA group (P=0.0223); qRT-PCR showed that the expression of GFAP in th e hippocampus of CIH group mice was significantly higher than that of RA group mice (P=0.0175); The levels of TNFα (P=0.02), IL-6 (P=0.0492), and IL-1β (P=0.0473) in the hippocampus of CIH mice increased compared to the RA group by Elisa. Conclusions: Chronic intermittent hypoxia for 4 weeks may induce short-term memory impairment in mice by inducing hippocampus inflammation. [ABSTRACT FROM AUTHOR]

Ferroptosis is a novel form of programmed cell death that relies on the accumulation of intracellular iron ions, causing irreversible damage to cell membranes through extensive lipid peroxidation, ultimately leading to cell death. Ferroptosis is closely associated with various neurodegenerative diseases. The ferroptosis of glial cells can regulate neuronal death by inducing neuroinflammation and affecting oxidative stress, thereby exacerbating the progression of neurodegenerative diseases. This review summarizes how ferroptosis occurs in different types of glial cells and its impact on neurons, aiming to deeply understand the effects of glial cell ferroptosis on neurodegenerative diseases and explore the potential therapeutic applications of inhibiting this process in treatment. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effects of Panax notoginseng compound formula（ PN） on endometrial fibrosis by regulating inflammatory reaction and intestinal flora （IF） in a rat model of intrauterine adhesion （IUA）. METHODS: The rat IUA model was established by following the mechanical injury method. A total of 50 rats were randomly divided into sham group, model group, low-dose （210 mg/kg） PN group, medium-dose （420 mg/kg） PN group and high-dose （840 mg/kg） PN group. After 8 weeks of intragastric administration, the uterus was collected to observe morphological changes with naked eye. The degree of uterine tissue damage and fibrosis was evaluated through hematoxylin-eosin（ HE） and Masson staining. The collagen type I （Col I） was detected by immunohistochemistry. The interleukin-6（ IL-6） and IL-10 protein expression was detected by Western blot. The levels of IL-6, IL-1β, tumor necrosis factor-α （TNF-α） and vascular endothelial growth factor B （VEGFB） were detected by enzyme-linked immunosorbent assay （ELISA）. The IF diversity and population structure were observed by 16S amplicon. RESULTS: Compared with the sham group, the uteruses of rats in the model group showed: reduced elasticity, accompanied by congestion and edema; decreased number of glands and blood vessels, and thinned endometrium（ P<0. 01）; increased collagen fibers and Col I protein expression（ P<0. 01）; significantly increased IL-1β, IL-6, TNF-α and VEGFB levels in the uterine tissue （P<0. 01）; decreased IL-10 level （P< 0. 01）; and reduced IF diversity （P<0. 05）. Compared with the model group, the drug intervention groups exhibited: recovered elasticity of the uterus and relieved congestion and edema; increased number of endometrial glands and blood vessels （P<0. 05）; decreased collagen fibers and Col I protein expression （P<0. 01）; reduced IL-1β, IL-6, and TNF-α levels to varying degrees in the uterine tissue （P<0. 05）; elevated IL-10 level （P<0. 01）; and improved IF diversity （P< 0. 05）. CONCLUSION: The PN is able to significantly improve the endometrial tissue fibrosis in IUA rats. The underlying mechanisms may be related to the inhibition of IL-6, IL-1β and TNF-α expression, up-regulation of IL-10, and improvement of IF diversity. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effect of paeoniflorin （PF） on TLR4/MyD88 signaling pathway in liver of rats with metabolic dysfunction-associated fatty liver disease. METHODS: SPF grade male SD rats were randomly divided into four groups: normal control（ NC） group, model control（ MC） group, low-dose paeoniflorin（ PL） group, and highdose paeoniflorin （PH） group. The normal group was given standard diet, and the other three groups were given high-fat diet for 8 weeks. From the fifth week, rats in paeoniflorin groups were given low dose （25 mg·kg-1·d-1） or high dose （50 mg·kg-1·d-1） paeoniflorin for 4 weeks. Serum alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, total cholesterol（ TC） and triglyceride（ TG） were measured by biochemical method. The levels of tumor necrosis factor（ TNF）- α was detected by ELISA. Pathological change of the liver was detected with hematoxylin-eosin （HE） staining and oil red O staining, and evaluated semi-quantitatively with the nonalcoholic fatty liver disease activity score （NAS）. The expression levels of TLR4, MyD88 and phosphorylated nuclear factor （p-NF）-κB p65 in liver tissues were detected by immunohistochemistry and Western blot. RESULTS: Compared with the NC group, rats in the MC group showed increased TC, TG, ALT, AST and TNF-α in serum （P<0. 05）, and more lipid droplets in hepatocytes and inflammatory cell infiltration in the portal area, with higher NAS, TLR4, MyD88 and p-NF-κB p65 proteins in liver tissue （P<0. 05）. However, paeoniflorin could reduce TC, TG, ALT, AST and TNF-α in serum （P<0. 05）, improve histopathological changes of liver, decrease the NAS scoring（ P<0. 05）, and inhibit hepatic TLR4/MyD88/p-NF-κB p65 expressions（ P<0. 05）. CONCLUSION: Paeoniflorin could improve the lipid metabolism disorder and reduce liver inflammation during MAFLD, and the latter effect might be in part related to the inhibition of TLR4/MyD88 signaling pathway. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effect of Ganoderma leucocontextum extract（ GLE） on mice with cisplatininduced acute kidney injury （AKI） and lipopolysaccharide （LPS）-induced cellular inflammation. METHODS: Eightweek-old male C57BL/6 mice were randomly divided into control group, AKI group, low-dose （100 mg/kg） GLE group, high-dose（ 300 mg/kg） GLE group, and quercetin（ 100 mg/kg） group, with 6 mice in each group. The AKI model was established by intraperitoneal injection of a 20 mg/kg cisplatin solution. After GLE intervention for 3 d, serum creatinine （SCr） and blood urea nitrogen （BUN） levels were measured. Renal pathology was observed using HE and PAS staining. The expression of β-catenin and Axin2 protein in each group was detected by immunohistochemistry. The expression levels of interleukin-1β （IL-1β）, IL-6, β-catenin and Axin2 in each group were detected by Western blot and RT-qPCR. The TCMK1 cells were stimulated with 2 mg/L LPS to simulate cellular inflammatory injury. After GLE treatment （0. 2, 0. 4, 0. 6 and 0. 8 g/L） for 24 h, the expressions of IL-1β, IL-6, β-catenin and Axin2 in each group were detected. Further overexpression of Axin2 was used to verify the changes in the above-mentioned indices. RESULTS: High doses of GLE significantly reduced SCr （P<0. 01） and BUN （P<0. 05） levels compared with the AKI mice. AKI mice showed renal tubule dilatation, tubular epithelial cell necrosis, vacuolation, and other pathological manifestations, which were improved after GLE intervention. Immunohistochemistry showed increased expression of Axin2 and β-catenin protein in the kidneys of AKI mice, which was reduced by GLE intervention. Western blot and RT-qPCR results in vitro and in vivo showed that GLE intervention significantly inhibited the expression and mRNA levels of IL-1β, IL-6, Axin2 and β-catenin （P<0. 05）. Overexpression of Axin2 antagonized the effect of GLE on IL-1β, IL-6, Axin2 and β-catenin, resulting in significantly up-regulated expressions of these proteins and mRNAs （P<0. 01）. CONCLUSION: GLE significantly alleviates the inflammatory response in AKI mice and LPS-induced cells, and protects against cisplatin-induced kidney injury in mice by inhibiting the Axin2/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

AIM: This study aimed to investigate the effects of sinomenine hydrochloride （SIN） on the ultrastructure of renal tissue and the expression of interferon gene-stimulating factor in db/db mice. METHODS: Sixteen 12-week-old male db/db mice were randomly divided into two groups: a model group and a sinomenine hydrochloride （SIN） group, each consisting of 8 mice. An additional 8 wild-type （WT） mice served as the normal control group. The sinomenine hydrochloride group was administered the treatment for 8 weeks, followed by a 20-week observation period, while the normal and model groups received an equal volume of saline via gavage. Weekly measurements were taken for body weight and fasting blood glucose. Serum creatinine （SCr） and blood urea nitrogen （BUN） levels were assessed, and 24-hour urinary microalbumin（ ALB） levels, as well as serum inflammatory cytokines interleukin-1β（ IL-1β）, IL-6 and tumor necrosis factor-α （TNF-α）, were determined using ELISA. Pathological changes in renal tissue were evaluated through hematoxylin-eosin （HE） staining, while ultrastructural alterations were examined using transmission electron microscopy. Immunohistochemistry and Western blotting were employed to assess STING protein expression in renal tissue, and STING mRNA expression was quantified via RT-qPCR. RESULTS: Compared to the normal group, the model group exhibited significant increases in BUN, ALB, and SCr levels （P<0. 01）, alongside elevated inflammatory markers IL-1β, IL-6, and TNF-α （P<0. 01）. Notable pathological changes included leukocyte wall thickening in capillaries, inflammatory cell infiltration, increased mesangial matrix, disorganized and linear alignment of podocytes, and thickening of the basement membrane. Moreover, STING protein and mRNA expression levels were significantly elevated （P<0. 01）. In contrast, the sinomenine hydrochloride group demonstrated significantly reduced levels of renal function markers （BUN, ALB and SCr） compared to the model group （P<0. 01）, as well as decreased concentrations of inflammatory factors IL-1β, IL-6, and TNF-α （P<0. 01）. Improvements in renal histopathology included decreased leukocyte wall thickening, reduced inflammatory cell presence, diminished mesangial matrix, and a significant reduction in foot process fusion, alongside thinner basement membranes. Both STING protein and mRNA expression levels were also significantly lower （P<0. 01）. CONCLUSION: Sinomenine hydrochloride effectively mitigates renal tissue injury, improves ultrastructural alterations, and inhibits inflammatory responses in db/db mice. Its mechanism of action appears closely linked to the downregulation of STING protein and mRNA expression. [ABSTRACT FROM AUTHOR]

In the study of cardiovascular diseases, Peroxiredoxin 6 (PRDX6) is the only mammalian 1-Cys member of the Peroxiredoxin (PRDX) family and has attracted much attention. PRDX6 plays a unique role in oxidative stress due to its peroxidase activity and phospholipase A2 activity, and has been shown to participate in redox homeostasis and phospholipid metabolism. In recent years, the role of PRDX6 in the occurrence and development of cardiovascular diseases has received great attention. However, there is no unified understanding of the function of PRDX6 in the cardiovascular system at present. This article aims to briefly summarize the research progress of PRDX6 in cardiovascular diseases such as atherosclerosis, pulmonary hypertension, myocardial infarction, heart failure, abdominal aortic aneurysm, and systematically review the expression changes, mechanism of action, and possible therapeutic potential of PRDX6 in these cardiovascular diseases, hoping to provide new ideas and strategies for cardiovascular diseases intervention. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic vascular disease primarily affecting large and medium-sized arteries, involving multiple complex pathogenic factors. In recent years, numerous research trends in atherosclerosis, such as inflammation, gut microbiota, pyroptosis, ferroptosis, autophagy, cuproptosis, exosome and non-coding RNA have emerged. This article aims to review the recent advancements in these research directions, with the hope of opening new avenues for the mechanism of atherosclerosis and the treatment of diseases related to atherosclerosis. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVD) are the leading cause of death among residents in China and significantly impact patients’ quality of life. The pathogenesis of CVD is complex, with chronic low-grade inflammation as a predominant feature. The nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is a key regulator of inflammatory responses and plays a crucial role in innate immune responses. Its abnormal activation leads to excessive inflammation and pyroptosis, which is closely associated with the development of atherosclerosis, myocardial infarction, diabetic cardiomyopathy, and other CVDs. Recent studies suggest that exercise, as a safe and effective non-pharmacological intervention, can mitigate cardiovascular inflammation and pyroptosis by inhibiting NLRP3 inflammasome activation, thereby playing a positive role in CVD prevention and treatment. However, the theories and mechanisms of exercise-mediated NLRP3 inflammasome intervention in CVD remain underexplored. Therefore, this review summarizes the relationship between the NLRP3 inflammasome and CVD, explores the effects of different types, intensities, and durations of exercise on NLRP3 inflammasome activation, and provides a comprehensive analysis of the signaling pathways involved in exercise interventions targeting the NLRP3 inflammasome for the prevention and treatment of CVD. The aim is to provide new insights and references for exercise-based prevention and management of CVD. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effect and mechanism of action of Qizhu prescription in mice with non-alcoholic fatty liver disease （NAFLD）. Methods: A total of 60 male C57BL/6J mice were randomly divided into normal group， model group， low-dose Qizhu prescription group （4.75 g/kg）， middle-dose Qizhu prescription group （9.50 g/kg）， high-dose Qizhu prescription group （19.00 g/kg）， Yishanfu group （228 mg/kg）， with 10 mice in each group. After 16 weeks of modeling with a high-fat high-cholesterol diet and 20% fructose water， each group was given the corresponding drug once a day for 8 weeks. The serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein （LDL） were measured； ELISA was used to measure the serum levels of free fatty acid （FFA）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， superoxide dismutase （SOD）， and malondialdehyde （MDA）； HE staining and oil red O staining were used to the pathological changes of liver tissue； Western blot was used to measure the protein expression levels of LC3BⅡ/Ⅰ， p62/SQSTM1， Beclin-1， and Drp1， and real-time PCR was used to measure the mRNA expression levels of Drp1， Beclin-1， and p62/SQSTM1. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. Results: Compared with the normal group， the model groups had significant increases in the serum levels of TG， TC， ALT， AST， LDL， FFA， TNF-α， IL-1β， and MDA and a significant reduction in the serum level of SOD （P<0.05）. HE staining showed that the mice in the model group had hepatocyte steatosis and a large number of fat vacuoles in liver tissue， and oil red O staining showed that the mice in the model group had a large number of red lipid droplets of varying sizes in hepatocytes， with a significant increase in the percentage of oil red O staining area compared with the normal group （P<0.05）. Real-time PCR showed that compared with the normal group， the model group had significant increases in the mRNA expression levels of Drp1 and Beclin-1 and a significant reduction in the mRNA expression level of p62/SQSTM1 in liver tissue （all P<0.05）， and Western blot showed that compared with the normal group， the model group had significant increases in the protein expression levels of Drp1， Beclin-1， and LC3BⅡ/Ⅰ and a significant reduction in the protein expression level of p62/SQSTM1 in liver tissue （all P<0.05）. Compared with the model group， some Qizhu prescription groups and the Yishanfu group had significant reductions in the serum levels of TG， TC， ALT， AST， LDL， FFA， TNF-α， IL-1β， and MDA and a significant increase in the serum level of SOD （all P<0.05）. Compared with the model group， each administration group had a significant improvement in steatosis of liver tissue， a significant reduction in the percentage of oil red O staining area， significant reductions in the mRNA expression levels of Drp1 and Beclin-1， and a significant increase in the mRNA expression level of p62/SQSTM1 （all P<0.05）； there were significant reductions in the protein expression levels of Drp1， Beclin-1， and LC3BⅡ/Ⅰ， while some administration groups had a significant increase in the protein expression level of p62/SQSTM1 （all P<0.05）， with a significantly better effect in the middle- and high-dose Qizhu prescription groups （all P<0.01）. Conclusion: Qizhu prescription improves lipid metabolism and inflammation in mice with NAFLD possibly by regulating hepatocyte mitophagy. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect and mechanism of Wanxuandi Ointment (WXD) on imiquimodinduced psoriasis in mice. Methods A psoriasis mice model was established by applying imiquimod to the hairless area on the back of the mice for 7 consecutive days. In the study of the time-effect relationship, mice were randomly separated into normal group, model group, groups of 1st, 2nd, 3rd, 4th day of WXD-medication, and mometasone furoate (MF) group. The corresponding ointment was rubbed into the skin once daily. In the study of dose-effect relationship, mice were randomly separated into normal group, model group, groups of 1, 2, 3 time of WXD-medication, and MF group. These drugs were rubbed into the skin at the 4th day of modeling. The psoriasis area and severity index (PASI) and pathological observation were used to evaluate the effect of WXD on psoriasis. The mRNA expressions of TNF-α and IL-1β in the skin were detected by qRT-PCR. The content of IL-23, IL-17A, 5-HT and histamine were detected by ELISA. The protein expressions of myeloperoxidase (MPO) and p-JAK2 in the skin were detected by immunohistochemistry. The protein expression of p-STAT3 was detected by Western Blot. Results The results of time-effect relationship showed that PASI, thickness of stratum spinosum, length of drumstick-shaped protrusion of stratum spinosum, area of drumstick-shaped protrusion of stratum spinosum /stratum spinosum area were obviously reduced in groups of 1st, 2nd, 3rd, 4th day of WXD-medication (P＜0.05, P＜0.01). The results of dose-effect relationship suggested that all above mentioned indexes in group of 1 time of WXD-medication were also significantly decreased (P＜0.05, P＜0.01). Additionally, WXD significantly reduced the protein expression of MPO, p-JAK2, p-STAT3, IL-23 and IL-17A, and the mRNA expressions of TNF-α and IL-1β in skin tissues of psoriasis mice, as well as the serum levels of 5-HT and histamine (P＜0.05, P＜0.01). Conclusion WXD administration for prevention during the model establishment and therapeutic treatment of WXD in the stage of obvious psoriasis symptoms are effective, once-daily administration of WXD is considered be the best treatment for psoriasis. The possible mechanism is related to inhibiting inflammatory response by down-regulating JAK2/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective This study aims to investigate the effect of resveratrol on neuronal damage in rats with acute cerebral infarction (ACI) by regulating the high-mobility group protein B1 (HMGB1) /Toll-like receptor 4 (TLR4) / nuclear factor-κB (NF-κB) signaling pathway. Methods Rats were randomly separated into blank group, infarction group, resveratrol group, HMGB1 activator (recombinant rat HMGB1 protein, rRHMGB1) group, and resveratrol+ rRHMGB1 group, with 18 rats in each group. Except for the blank group, rats in all other groups were used to construct ACI models using the method of middle cerebral artery occlusion. Drug treatment began at 1 hour after successful modeling, once a day, for 7 days. Changes in neurological impairment score and cerebral infarction volume coefficient were detected. ELISA was applied to detect levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in infarction region of brain tissue. Nissl staining was applied to detect the number of surviving neurons in infarction region of brain tissues. TUNEL staining was applied to detect neuronal apoptosis in infarction region of brain tissue. Western Blot was applied to detect Bcl2 associated X protein (Bax), TLR4, Cleaved Caspase-3, HMGB1, and p-NF-κB p65 protein in brain tissue. Results Compared with the blank group, the neurological damage score, cerebral infarction volume coefficient, levels of TNF- α, IL-1β, IL-6 in the infarction region of brain tissue, neuronal apoptosis rate, Bax, TLR4, Cleaved Caspase-3, HMGB1, p-NF- κB p65 protein increased in the infarction group, while the number of surviving neurons in the infarction region of brain tissue decreased (P＜0.05). Compared with the infarction group, the neurological damage score, cerebral infarction volume coefficient, levels of TNF-α, IL-1β, IL-6 in the infarction region of brain tissue, neuronal apoptosis rate, and protein expression of Bax, TLR4, Cleaved Caspase-3, HMGB1, p-NF- κB p65 decreased in resveratrol group and resveratrol+rRHMGB1 group, the number of surviving neurons in the infarction region of brain tissue increased (P＜0.05). Change of the corresponding indicators in the rRHMGB1 group was opposite to that in the resveratrol group (P＜0.05). Compared with the resveratrol group, the neurological damage score, cerebral infarction volume coefficient, levels of TNF-α, IL-1β, IL-6 in the infarction region of brain tissue, neuronal apoptosis rate, the protein expression of Bax, TLR4, Cleaved Caspase-3, HMGB1, p-NF-κB p65 increased in the resveratrol+rRHMGB1 group, the number of surviving neurons in the infarction region of brain tissue decreased (P＜0.05). Conclusion The mechanism by which resveratrol improves neuronal damage in ACI rats may be related to the inhibition of the HMGB1/TLR4/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of ophiopogonin D on myocardial in rats with ischemia-reperfusion injury (MIRI) by regulating the sphingosine kinase 1 (SphK1) /sphingosine 1-phosphate (S1P) /sphingosine 1-phosphate receptor 1 (S1PR1) pathway. Methods Rats were randomly separated into MIRI group, ophiopogonin D group, SphK1 activator (K6PC-5) group, ophiopogonin D+K6PC-5 group, and sham group, with 12 rats in each group. Except for the sham group, MIRI models were constructed by ligating the left anterior descending coronary artery of rats in all other groups. After successful modeling, medication treatment was carried out immediately, once a day for 2 weeks. The ultrasound imaging system was applied to evaluate changes in left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in rats. HE staining was applied to detect the pathology of myocardial tissue. ELISA was applied to detect levels of creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in myocardial tissue. TUNEL staining was applied to detect myocardial cell apoptosis in myocardial tissue. Immunohistochemical staining was applied to detect the proportions of Bim and Caspase-3 positive cells in myocardial tissue. Western Blot was applied to detect S1P, SphK1, and S1PR1 proteins in myocardial tissue. Results Compared with the sham group, rats in the MIRI group showed myocardial structural damage, disordered fiber arrangement, decreased myocardial cells, nuclear pyknosis, and a large number of inflammatory cell infiltration. The LVFS and LVEF decreased, the levels of CK-MB, LDH, IL-1β, TNF- α, myocardial cell apoptosis rate, proportions of Bim and Caspase-3 positive cells, and S1P, SphK1, and S1PR1 proteins in myocardial tissue were elevated (P＜0.05). Compared with the MIRI group, the rats in the ophiopogonin D group showed relief of above-mentioned phenomenon, including myocardial structural damage, disordered fiber arrangement, decreased myocardial cells, nuclear pyknosis, and infiltration of a large number of inflammatory cells. The LVFS and LVEF increased, the levels of CK-MB, LDH, IL-1β, TNF-α, myocardial cell apoptosis rate, proportions of Bim and Caspase-3 positive cells, and S1P, SphK1, and S1PR1 proteins in myocardial tissue decreased (P＜0.05). K6PC-5 reversed the effects of ophiopogonin D on cardiac dysfunction, myocarditis, and myocardial cell apoptosis in MIRI rats. Conclusion The mechanism by which ophiopogonin D inhibits myocarditis and myocardial cell apoptosis in MIRI rats may be related to the inhibition of the SphK1/S1P/S1PR1 pathway. [ABSTRACT FROM AUTHOR]

Sepsis is a severe and life-threatening symptom that poses a significant risk to human health. Treatment mainly involves supportive care, but research on new drugs is ongoing. Advancements have been achieved in the management of immune function, inflammatory pathway, blood coagulation, and vascular endothelial homeostasis in sepsis. The advances in the treatment of sepsis in recent years were these reviewed in this article. [ABSTRACT FROM AUTHOR]

The aryl hydrocarbon receptor (AhR), also known as dioxin receptor, is a ligand-dependent transcription factor. Because of its important role in occurrence and development of cancer, it has been widely studied. AhR is now considered to be an important regulator of host-environment interactions in immune and inflammatory responses and is involved in pathogenesis of many skin diseases. Because AhR is highly expressed in all types of skin cells and regulates many genes that are critical to skin function, it has the potential to be a new target for the treatment of inflammatory skin diseases. This paper presents and analyzes research findings on the relationship between AhR and inflammatory skin diseases to help accelerate the development of new drugs. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of sufentanil (suf) on hepatic injury in burn sepsis rats by regulating Janus kinase 2 (JAK2)/signal transduction and transcriptional activator 3 (STAT3) signaling pathway. Methods SD rats were randomly divided into the control group, the model group, the suf low-dose group (0.75 µg/kg), the suf high-dose group (3 µg/kg), the imipenem group (90 mg/kg) and the suf high-dose + kumamycin group (3 µg/kg suf+4 mg/kg kumamycin). Serum liver function indexes including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. The pathological changes of liver tissue were observed by HE staining. The contents of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-6 were detected by enzyme-linked immunosorbent assay (ELISA). Terminal deoxynucleotide transferase mediated dUTP nick end labeling (TUNEL) staining was used to detect hepatocyte apoptosis. Western blot assay was used to detect the expression of p-JAK2 and p-STAT3 proteins in liver tissue. Results Compared with the control group, the model group showed elevated serum levels of ALT and AST, swelling of liver cells and infiltration of numerous inflammatory cells in liver tissue. The levels of TNF-α, MCP-1 and IL-6 in liver tissue, apoptosis rate of liver cells, and expression levels of p-JAK2 and p-STAT3 proteins were increased (P＜0.05). Compared with the model group, serum levels of ALT and AST were reduced in the suf low-dose group and the suf high-dose group, and pathological damages of liver tissue were improved. The contents of TNF- α, MCP-1 and IL-6 in liver tissue, the apoptosis rate of liver cells, and the expression levels of p-JAK2 and p-STAT3 proteins were reduced (P＜0.05). Moreover, changes in above indicators were significantly higher in the suf high dose group of suf than those in the suf low dose group (P＜0.05), and there was no significant difference compared with the imipenem group. Kumamycin inhibited the improvement effect of high-dose suf on liver injury in rats with burn sepsis (P＞0.05). Conclusion Sufentanil may improve liver injury in burn-induced sepsis rats by inhibiting the JAK2/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the improvement effect and related mechanism of roxadustat on myocardial ischemia-reperfusion (I/R) injury in mice. Methods Twenty four male C57BL/6N mice were randomly divided into the sham operation group, the control group and the roxadustat group, with eight mice in each group. A mouse myocardial I/R model was established. The control group was given 100 µL saline injection containing 5% dimethyl sulfoxide by gavage. The roxadustat group was given 25 mg/kg roxadustat by gavage. The left anterior descending coronary artery of mice in both groups was ligated for 40 minutes, and then reperfusion for 24 hours to establish the myocardial I/R model. In the sham operation group, only the left anterior coronary artery was pierced without ligation. The area of myocardial infarction in mice was detected by triphenyltetrazolium chloride (TTC) staining. The apoptosis of mouse cardiomyocytes was detected by TdT-mediated dUTP nick and labeling (TUNEL) staining. The expression of apoptosis-related proteins bcl-2 associated X protein (Bax), Caspase3 and inflammatory cell markers F4/80 and myeloperoxidase (MPO) were detected by immunohistochemistry staining. The damage of myocardial cells was observed by hematoxylin-eosin (HE) staining. Results The area of myocardial infarction after myocardial I/R was reduced in the roxadustat group compared to the control group and the sham operation group (P＜0.05). The number of apoptotic cells was higher in the control group and the roxadustat group than that in the sham operation group, and the number of apoptotic cells was lower in the roxadustat group than that in the control group (P＜ 0.05). The expression levels of Bax and Caspase3 proteins in myocardial tissue were higher in the control group and the roxadustat group than those in the sham operation group, while those of the roxadustat group was lower than those of the control group (P＜0.05). The expression levels of F4/80 and MPO proteins in myocardial tissue were lower in the roxadustat group than those in the control group (P＜0.05). In the control group, the myocardial tissue arrangement was disordered, and there was an increase in interstitial vacuoles. Compared with the control group, the myocardial cells were arranged more neatly in the roxadustat group, and the interstitial vacuoles were reduced. Conclusion Roxadustat can reduce the myocardial infarction area after I/R injury, inhibit myocardial cell apoptosis, alleviate myocardial injury, reduce infiltration of myocardial macrophages and neutrophils, and reduce inflammatory injury. [ABSTRACT FROM AUTHOR]

Endoplasmic reticulum stress refers to a cellular stress response triggered when cells are stimulated, which is manifested as the disruption of endoplasmic reticulum homeostasis and dysfunction in various pathological conditions, resulting in the accumulation of a large number of misfolded and unfolded proteins within the endoplasmic reticulum and an imbalance of calcium ions. Macrophages are the most abundant immune cells in the liver and play an important role in maintaining liver homeostasis and various liver diseases. Recent studies have confirmed that the unfolded protein response caused by endoplasmic reticulum stress plays an important role in regulating macrophage immune response. This article reviews the mechanisms of endoplasmic reticulum stress regulating macrophage immune response and its role in liver diseases such as ischemia-reperfusion injury during organ transplantation, liver fibrosis, and hepatocellular carcinoma, in order to deepen the understanding of the mechanism of macrophage immune regulation and provide new ideas for research and interventional treatment related to liver diseases. [ABSTRACT FROM AUTHOR]

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Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

AIM: To analyze the expression profiles of long non-coding RNAs （lncRNAs） in the aortas of atherosclerotic mice, and explore the role and mechanism of lncRNA AI662270 in regulating macrophage inflammation and lipid phagocytosis. METHODS: Twenty 8-week-old male apolipoprotein E gene knockout （ApoE-/-） mice were randomly divided into experimental and control groups, with 10 mice in each group. The experimental group was fed a high-fat diet for 12 weeks to induce atherosclerosis, while the control group received a normal diet. Body weight and blood lipid levels were measured, and atherosclerotic lesions were detected using Oil Red O staining. High-throughput RNA sequencing （RNA-seq） was used to analyze the lncRNA expression profiles in mouse aortas, and differentially expressed lncRNAs were validated by RT-qPCR. Antisense oligonucleotides （ASO） were used to knock down the expression of lncRNA AI662270 in mouse macrophage RAW264. 7 cells. Six treatment groups were established: blank（ no treatment） group, oxidized low-density lipoprotein（oxLDL） group （80 mg/L oxLDL）, negative control ASO （ASO-NC） group （transfected with ASO-NC）, oxLDL+ASO-NC group （transfected with ASO-NC and treated with 80 mg/L oxLDL）, ASO-AI662270 group（ transfected with ASO-AI662270）, and oxLDL+ASO-AI662270 group（ transfected with ASO-AI662270 and treated with 80 mg/L oxLDL）. Tumor necrosis factor-α （TNF-α） and interleukin-6（IL-6） levels were measured using Enzymelinked immunosorbent assay （ELISA）. NF-κB p65, pNF-κB p65, IκBα and pIκBα levels were detected by Western blot, and NF-κB p65 in the cell nucleus was examined using fluorescent probes. RESULTS: The atherosclerosis mouse model showed significant differences in body weight, serum lipids, and aortic plaque area compared to the control group （P< 0. 01）. A total of 29 differentially expressed lncRNAs were identified involved in metabolic pathways, autophagosome formation, and cell adhesion molecule expression （P<0. 05）. LncRNA AI662270 was significantly upregulated in lesions and oxLDL-stimulated macrophages（ P<0. 05）. Knockdown of AI662270 significantly reduced TNF-α and IL-6 expression in oxLDL-induced RAW264. 7 cells（ P<0. 01）, suppressed lipid phagocytosis, and inhibited pNF-κB p65 and pIκBα expression （P<0. 05）. Additionally, the knockdown of AI662270 reduced the nuclear content of NF-κB p65. CONCLUSION: The lncRNA expression profiles in the aortas of atherosclerotic mice were significantly altered. LncRNA AI662270 is crucial in modulating inflammation and lipid phagocytosis in mouse macrophages through the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Objective Pulmonary oxygen poisoning resulting from hyperbaric oxygen, frequently occurs in specialized operations, without any current effective prevention or treatment measures. To elucidate the impact and mechanism of neostigmine (NEO) in combination with anisodamine (ANI) (neoscopolamine) on pulmonary oxygen toxicity. Methods The animal model of pulmonary oxygen poisoning was established. C57BL/6 mice were exposed to 2.5 ATA 99.9% oxygen for 6 h. The control group mice were injected with normal saline ip, while the treatment group mice received injections of ANI (25 mg/kg, ip）and NEO (50 μg/kg, ip）. Lung tissues were collected and stained with HE to observe any pathological injuries after exposure. Evans blue stain was utilized to identify lung permeability, wet/dry lung ratio, and protein concentration in the bronchoalveolar lavage fluid (BALF) to assess the lung injury’s severity. The modifications in inflammatory factors, oxidative stress indicators, and iron content in lung tissue were assessed. Results The results showed that the 2.5 ATA 99.9% oxygen-exposed group experienced a significant worsening of lung injury, as well as increased lung permeability, lung wet/dry ratio, and protein content in alveolar lavage fluid when compared to the control group. Moreover, mRNA levels of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, and IFN-γ in the lung tissue of the model group were significantly elevated, while the levels of anti-inflammatory cytokines IL-4 and TGF-β were significantly reduced. The oxidative index MDA also significantly increased, while the antioxidant index GSH significantly decreased. Additionally, the expression of GPX4, a marker of ferroptosis, increased with an increase in iron content. Neoscopolamine treatment successfully reversed those effects. Conclusion The combined use of ANI and NEO had a protective effect on pulmonary oxygen poisoning. Neoscopolamine may inhibit inflammation and oxidative stress by activating the cholinergic anti-inflammatory pathway, thereby reducing the content of free iron in lung tissue and finally inhibiting cell ferroptosis. [ABSTRACT FROM AUTHOR]

To elucidate the potential mechanism of Wuji powder in treating polycystic ovary syndrome (PCOS), this study utilized TCMSP database to screen the active ingredients of each constituent drug in Wuji powder. Subsequently, we predicted the target proteins associated with these active ingredients. In parallel, we employed the GeneCards database to identify genes related to PCOS and determined the intersection of drug targets and disease targets using the online tool available at http://bioinformatics.psb.ugent.be/webtools/Venn/. The shared genes were considered as the target proteins of Wuji powder in the treatment of PCOS. Utilizing the String website, we constructed a protein-protein interaction (PPI) network diagram and identified key protein modules and hub genes within the PPI network using Cytoscape 3.7.1 software. Further analysis in the DAVID database involved GO and KEGG pathway enrichment analyses of the genes within the identified key modules. Our investigation revealed a total of 63 active ingredients in Wuji powder with potential therapeutic effects on PCOS, corresponding to 266 drug targets. Intersection with PCOS-related disease targets yielded 174 shared targets. Ten key modules and ten hub genes (TNF, MMP9, AKT1, ECG, VEGFA, PTGS2, IL-6, MAPK3, STAT3, and CXCL8) were identified through network analysis. KEGG pathway enrichment analysis uncovered 58 signaling pathways, including TNF, MAPK, and PI3K-Akt signaling pathways. GO functional annotation delineated five cellular components (CC), nine molecular functions (MF), and 58 biological processes (BP). Noteworthy findings included extracellular space, enzyme binding, and drug response among CC, MF, and BP categories, respectively. These results collectively suggested that Wuji powder might exert its therapeutic effects on PCOS by modulating the TNF/PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Heart failure with preserved ejection fraction (HFpEF) is a significant challenge in the field of cardiovascular diseases. Inflammation, myocardial fibrosis, and coronary microcirculation dysfunction are the core pathophysiological mechanisms of HFpEF. As a key part of adaptive immune response, T cell subsets widely participate in the above process through various mechanisms, further aggravating the damage of myocardial structure and function, and ultimately leading to the development of HFpEF. This article provides a comprehensive review on the roles of immunity and inflammation in HFpEF, summarizes the characteristics and functions of different T cell subsets involved in HFpEF, and aims to explore novel biomarkers and potential therapeutic targets by targeting T cell subsets. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the mechanism of therapeutic effect of pucrarin on Hyperlipidemia (HLP) model mice, C57BL/6J mice were randomly divided into blank Control group (Control), disease Model group (Model) and puerarin low-dose, medium-dose and high-dose groups (PUE-L, PUE-M, PUE-H). After the successful construction of the hyperlipidemia model, the mice were treated with puerarin for 4 weeks, and the changes of the lipid profile of the mice were detected by the kit. In addition, pathological changes of mouse liver tissues were observed, and key proteins in liver tissues were detected by Western blot. They included the expression levels of adenylate activated protein kinase (AMPK) and rapamycin mammalian target protein (mTOR) signaling pathway, sterol regulatory element binding protein (SREBP), a key regulatory protein of lipid metabolism, and microtubule-associated protein light chain 3 (LC3) and autophagy substrate (P62) during autophagy, Further, we used quantitative polymerase chain reaction (q-PCR) to detect the mRNA expression of acetyl-CoA carboxylase (ACC), fatty acid synthetase (FAS), sterol regulatory element-binding protein-1c (SREGBP-1C) in liver tissue. And the expression levels of mRNA and inflammatory factors related to AMPK/mTOR signaling pathway. Compared with the model group, the levels of total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) in the serum of puerarin treated group were significantly decreased, while the levels of high density lipoprotein cholesterol (HDL-C) were significantly increased. In liver tissue, the vacuole-like changes and lipid droplet accumulation were significantly reduced after puerarin intervention, After administration, the relative expression levels of ACC, FAS and SREBP-Ic mRNA in liver tissue decreased, the expression levels of LPS and pro-inflammatory factors TNF-α and II-8 decreased, while the expression levels of antiinflammatory factors 11-4 and 11-10 increased. In addition, the protein levels of mTOR, SREBP and P62 were decreased, while the expression levels of AMPK, p-AMPK and LC3 were increased. In summary, the experimental results show that puerarin can effectively improve the blood lipid profile of hyperlipidemia model mice and reduce the inflammatory response. The mechanism of action may be related to the regulation of AMPK/mTOR signaling pathway by puerarin, which promotes the activation of autophagy. These findings provide a new perspective on the treatment of hyperlipidemia, especially in the use of plant medicine. [ABSTRACT FROM AUTHOR]

Nonalcoholic steatohepatitis (NASH) is a liver disease closely associated with metabolic syndrome, and its pathogenesis includes insulin resistance, lipid metabolism disorders, and inflammatory response. This article briefly describes how CD8+ T cells exert a cytotoxic effect through the three pathways of the Fas-Fas ligand signaling pathway, the release of perforin and granzymes, and the secretion of tumor necrosis factor- α and other cytokines, and these mechanisms allow CD8+ T cells to specifically kill virus-infected cells and tumor target cells, thereby participating in immune regulation. At the same time, this article summarizes that CD8+ T cells promote the recruitment of macrophages cooperate with natural killer T cells to participate in the development of adipose tissue inflammation, and lead to liver injury through automatic attack and epigenetic mechanisms, finally promoting the pathogenesis of NASH. It is concluded that CD8+ T cells may become a new therapeutic target for NASH, and in-depth research on the specific mechanism of CD8+ T cells affecting the pathogenesis in NASH in the future may help to further guide clinical treatment. [ABSTRACT FROM AUTHOR]

Copyright of Modern Food Science & Technology is the property of Editorial Office of Modern Food Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Acupuncture & Tuina Science is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Various proteins, signaling pathways, and inflammatory mediators are involved in the pathophysiological process of osteoarthritis. The development of small molecule drugs targeting these proteins, signaling pathways, and inflammatory mediators can effectively delay the progression of osteoarthritis and ameliorate its clinical manifestations. OBJECTIVE: To review the research progress of small molecule drugs in the treatment of osteoarthritis based on the pathogenesis of osteoarthritis. METHODS: PubMed, CNKI, and WanFang databases were searched with English search terms “osteoarthritis, arthritis, osteoarthrosis, degenerative, arthritides, deformans, small molecule drugs, small molecule inhibitors, small molecule agents” and Chinese search terms “osteoarthritis, small molecule drugs, small molecule inhibitors.” A total of 68 articles were included for review according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION: (1) Currently, studies concerning the pathogenesis of osteoarthritis remain unclear. The occurrence and development of osteoarthritis are strongly associated with proteins, cytokines, and signal transduction pathways, so its therapeutic mechanism is relatively complex. Currently, targeting proteins, cytokines, and signal transduction pathways related to osteoarthritis with small molecule drugs has become a major research focus. (2) Small molecule drugs frequently possess visible intracellular or extracellular targets and efficacy, containing enhancing cartilage repair, resisting joint degradation, attenuating inflammation, and relieving pain. Other anti-osteoarthritis small molecule drugs have shown promise in promoting stem cell chondrogenic differentiation and cartilage matrix reconstruction. (3) At present, small molecule drugs targeting the pathophysiological process of osteoarthritis to delay the progression of osteoarthritis are still in the experimental stage, but most of these small molecule drugs have shown the expected results in the experimental process, and there are no relevant studies to illustrate the efficacy of small molecule drugs in the treatment of osteoarthritis. (4) Small molecule drugs for the treatment of osteoarthritis have reached the expected experimental results in the basic experimental stage. Numerous studies have exhibited that small molecule drugs can target the suppression of specific proteins, cytokines, and signal transduction pathways that cause osteoarthritis, so as to treat osteoarthritis. Nevertheless, its safety and effectiveness still need to be identified by further basic and clinical studies. This process needs to be investigated and studied by more scholars. (5) At present, many scholars in and outside China have made contributions to the treatment of osteoarthritis. Compared with traditional treatment methods, small molecule drugs reveal better efficacy and safety in the basic experimental stage, and it is expected to become an emerging method for the treatment of osteoarthritis in the future to rid patients of pain. [ABSTRACT FROM AUTHOR]

BACKGROUND: Lijin manipulation can promote skeletal muscle repair and treat skeletal muscle injury. However, the formation of fibrosis and scar tissue hyperplasia are closely related to the quality of skeletal muscle repair. To study the regulatory effect of Lijin manipulation on the formation of fibrosis and scar tissue hyperplasia is helpful to explain the related mechanism of Lijin manipulation to improve the repair quality of skeletal muscle injury. OBJECTIVE: To explore the mechanism of Lijin manipulation to improve the repair quality of skeletal muscle injury in rabbits, thereby providing a scientific basis for clinical treatment. METHODS: Forty-five healthy adult Japanese large-ear white rabbits were randomly divided into blank group, model group and Lijin group, with 15 rats in each group. Gastrocnemius strike modeling was performed in both model group and Lijin group. The Lijin group began to intervene with tendon manipulation on the 3rd day after modeling, once a day, and 15 minutes at a time. Five animals in each group were killed on the 7th, 14th and 21st days after modeling. The morphology and inflammatory cell count of gastrocnemius were observed by hematoxylin-eosin staining, the collagen fiber amount was observed by Masson staining, the expression of interleukin-6 and interleukin-10 in gastrocnemius was detected by ELISA. The protein and mRNA expressions of paired cassette gene 7, myogenic differentiation factor, myoblastogenin, alpha-actin, transforming growth factor beta 1, and type I collagen were detected by western blot and RT-PCR, respectively, and the expression of type I collagen protein was detected by immunohistochemistry. RESULTS AND CONCLUSION: Hematoxylin-eosin staining and Masson staining showed that compared with the model group, inflammatory cell infiltration and collagen fiber content decreased in the Lijin group (P < 0.01), and the muscle fibers gradually healed. ELISA results showed that compared with the model group, the expression of interleukin-6 in the Lijin group continued to decrease (P < 0.05), and the expression of interleukin-10 increased on the 7th day after modeling (P < 0.05) and then showed a decreasing trend (P < 0.05). Western blot and RT-PCR results showed that compared with the model group, the protein and mRNA expressions of paired cassette gene 7, myogenic differentiation factor, myoblastogenin in the Lijin group were significantly increased on the 14th day after modeling (P < 0.05), but decreased on the 21st day (P < 0.05); the protein and mRNA expressions of alpha-actin, transforming growth factor beta 1, and type I collagen in the Lijin group were significantly decreased compared with those in the model group (P < 0.05). Immunohistochemical results showed that the expression of type I collagen in the Lijin group was significantly lower than that in the model group (P < 0.05). To conclude, Lijin manipulation could improve the repair quality of skeletal muscle injury by inhibiting inflammation, promoting the proliferation and differentiation of muscle satellite cells, and reducing fibrosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: LncRNA-TNFRSF13C, an important factor in B cell development and function, is expressed in periodontal tissues of patients with periodontitis, but the specific mechanism is still unclear. OBJECTIVE: To investigate the mechanism of lncRNA-TNFRSF13C regulating miR-1246 on hypoxia-inducible factor 1α in periodontal cells. METHODS: Human periodontal ligament cells (hPDLCs) were treated with lipopolysaccharide and divided into group A (hPDLCs cell lines without transfection), group B (hPDLCs cell lines transfected with TNFRSF13C NC-siRNA), group C (hPDLCs cell lines transfected with TNFRSF13C-siRNA), group D (hPDLCs cell line transfected with miR-1246 mimics), group E (hPDLCs cell line transfected with miR-1246 siRNA), group F (hPDLCs cell line transfected with TNFRSF13C- siRNA+miR-1246 mimics), and group G (hPDLCs cell line transfected with TNFRSF13C-siRNA+miR-1246 siRNA). The relative expression of lncRNA-TNFRSF13C and miR-1246 in each group was detected by qRT-PCR. Cell counting kit-8 assay was used to detect cell viability. Apoptosis was detected by flow cytometry. Expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins was detected by western blot. The correlation between lncRNA- TNFRSF13C and miR-1246 was analyzed by Pearson, and the targeting relationship was analyzed by dual-luciferase reporter assay. RESULTS AND CONCLUSION: There was no significant difference in human periodontal ligament cell activity, apoptosis rate and protein indexes between groups A and B (P >0.05). Compared with group B, hPDLCS cell activity in group C was increased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were decreased (P < 0.05). Compared with group C, hPDLCS cell activity in group D was decreased, and apoptosis rate and the expression of hypoxia-inducible factor 1α and vascular endothelial growth factor proteins were increased (P < 0.05). Compared with group D, the cell activity of group E was increased (P < 0.05). The cell activity in group F was lower than that in group E, and the apoptosis rate was reduced in both groups E and F (P < 0.05). Compared with group F, the cell activity of group G was increased, and the apoptosis rate and the expression of hypoxia- inducible factor 1α and vascular endothelial growth factor were decreased (P < 0.05). LncRNA-TNFRSF13C was positively correlated with miR-1246 (P < 0.05). Compared with the TNFRSF13C-siRNA group, the fluorescence activity of miR-1246-wt in the TNFRSF13C-NC group was reduced (P > 0.05); compared with the miR-1246-NC group, the fluorescence activities of hypoxia-inducible factor 1α-wt and vascular endothelial growth factor-wt in the miR-1246 mimics group were increased (P < 0.05). To conclude, down-regulation of lncRNA-TNFRSF13C can promote the activity of periodontal cells treated with lipopolysaccharide, reduce apoptosis, and inhibit hypoxia-inducible factor 1α and vascular endothelial growth factor. The mechanism is related to the regulation of miR-1246 activity. [ABSTRACT FROM AUTHOR]