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Objective To investigate the effect of Kangxian Yiai Prescription (KXYA) on the mTOR/HIF-1α/VEGF signaling pathway in a rat model of precancerous lesions of liver cancer. Methods A total of 40 male Wistar rats were divided into normal group, model group, KXYA group, and Biejia Rangan Tablets (BJRG) group, with 10 rats in each group. The rats in the normal group were given intraperitoneal injection of normal saline at a dose of 0.4 mL/100 g, and those in the other three groups were given intraperitoneal injection of diethylnitrosamine at a dose of 50 mg/kg to establish a rat model of the precancerous lesions of liver cancer. Immunohistochemistry and Western Blot were used to measure the expression level of GST-Pi, and quantitative real-time PCR and Western Blot were used to measure the mRNA and protein expression levels of mTOR, HIF-1α, VEGF, PKM2, and GLUT1. A oneway analysis of variance or the Kruskal-Wallis H test 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 group had a significant increase in the protein expression level of GST-Pi in liver tissue (P<0.01), and compared with the model group, the KXYA group had a significant reduction in the protein expression level of GST-Pi (P<0.05). Compared with the normal group, the model group had significant increases in the mRNA expression levels of GLUT1 and PKM2 in liver tissue (P< 0.01), and compared with the model group, the BJRG group and the KXYA group had a significant reduction in the mRNA expression level of GLUT1（P<0.05). Compared with the normal group, the model group had significant increases in the protein expression levels of GLUT1 and PKM2 in liver tissue (P<0.01). Compared with the normal group, the model group had significant increases in the mRNA expression levels of mTOR, HIF-1α, and VEGF in liver tissue (P<0.01); compared with the model group, the BJRG group had significant reductions in the mRNA expression levels of mTOR and VEGF (P<0.05), and the KXYA group also had significant reductions in the mRNA expression levels of mTOR and VEGF (P<0.01). Compared with the normal group, the model group had significant increases in the protein expression levels of mTOR, HIF-1α, and VEGF in liver tissue (P<0.01); compared with the model group, the BJRG group had a significant reduction in the protein expression level of mTOR (P<0.01), and the KXYA group had significant reductions in the protein expression levels of mTOR, HIF-1α, and VEGF (P<0.05); compared with the BJRG group, the KXYA group had a significantly higher protein expression level of mTOR (P<0.01). Conclusion KXYA can inhibit the precancerous lesions of liver cancer by regulating the mTOR/HIF-1α/VEGF signaling pathway. [ABSTRACT FROM AUTHOR]

Recurrent spontaneous abortion (RSA) has a complex and diverse etiology, and many pathophysiological mechanisms of RSA remain unknown. In the reproductive system of women, reactive oxygen species (ROS) play an important role in hormone signaling, oocyte maturation, ovarian steroidogenesis, ovulation, luteal dissolution, luteal maintenance during pregnancy, embryo implantation, blastocyst development, reproductive cell function, and luteal formation. The abnormal expression of hypoxia inducible factor-1α, iron death, exposure to trace elements and heavy metals, and other factors directly or indirectly induce oxidative stress (OS). The imbalance between oxidative and antioxidant mechanisms has a negative impact on cell proliferation and apoptosis, leading to pathological phenomena such as cellular dysfunction, decreased biological activity, immune and inflammatory activation. The maternal -fetal interface plays a role in the exchange of gases, nutrients and metabolites during pregnancy, while producing various hormones and growth factors to support the normal development of the fetus and to maintain pregnancy. Therefore, OS in maternal-fetal interface is related to the occurrence and progression of RSA. [ABSTRACT FROM AUTHOR]

Liver regeneration plays a crucial role in the recovery after liver injury induced by N-acetyl-p-aminophenol (APAP) . After APAP overdose, the degree of regeneration increases with the extent of liver injury, leading to the resolution of liver injury and spontaneous recovery in most cases. However, severe APAP overdose can impair liver regeneration and result in uncontrolled liver injury, even failure to recover or death in severe cases. Following APAP-induced liver injury, interactions between cells in the liver are essential for regenerative response. Liver regeneration is jointly regulated by multiple proliferative signaling pathways, involving various kinases, nuclear receptors, transcription factors, and coactivators. Severe APAP overdose can inhibit the activation of proliferative signaling pathways, thereby causing cell cycle arrest and impairing liver regeneration. Although liver regeneration plays a critical role in the repair of APAP-induced liver injury, the underlying mechanisms remain unclear. This article reviews the research advances in the role of liver regeneration in APAP-induced liver injury, in order to provide a reference for further basic research in this area. [ABSTRACT FROM AUTHOR]

Objective To understand the research status and development trend in the field of molecular and cell biology of thyroid cancer. Methods Relevant literature published in the field of molecular and cell biology of thyroid cancer from January 1, 2013 to December 31, 2022 was obtained in the web of science core collection (WoSCC) according to the search conditions, and bibliometric and visual analysis were performed using the bibliometric software VOSviewer and Excel. Results A total of 1 627 literatures were included. Among them, 113 papers were published in 2013, and 214 were published in 2022. The annual number of publications was on the rise. There were 9 274 authors in total, of whom 6 published no less than 10 literatures. There were a total of 2 042 institutions, of which the top 10 institutions were mostly Chinese universities. There were 68 countries in total, and the largest number of publications was China, followed by the United States. There were 513 journals in total, and the top 10 journals with the largest number of literatures were mainly in the field of oncology, followed by the field of endocrinology and metabolism. A total of 62 563 references from 5 887 journals were cited. The most co-cited journal was Journal of Biological Chemistry (1 608 times), and the most co-cited references was Molecular Pathogenesis and Mechanisms of Thyroid Cancer (89 times). Conclusion The field of molecular and cell biology of thyroid cancer is currently developing steadily. Ferroptosis, glycosylation, telomerase reverse transcriptase and oxidative stress are the research frontiers in this field. [ABSTRACT FROM AUTHOR]

Neurokinin B (NKB) is a hypothalamic neuropeptide containing 10 amino acids and is an essential member of the tachykinin family. Based on studies in mammals, Kiss, NKB, and dynorphin A are located in the common neurons, named KNDy neurons, and NKB and Kiss can stimulate the GnRH pulses. In humans, the mutations of NKB and its receptor NK3R can lead to hypogonadotropic hypogonadism and infertility. NKB is also involved in many other physiological activities in mammals and has received increasing attention. NKB was first purified from porcine spinal cord extracts and named neurokinin B or neuromedin K. Subsequently, NKB has been identified in various species, and its encoding gene was named tac2 in ruminants and rodents, and tac3 in other mammals, birds, reptiles, amphibians, and fish. In teleosts, the NKB system was first identified in zebrafish by three laboratories in 2012; it was also found in grass carp, goldfish, Nile tilapia, European eel, orange-spotted grouper, and half-smooth tongue.As teleosts have experienced the third round of genome duplication (3R), the bony fish have two forms of tac3 genes, namely tac3a and tac3b. However, only tac3a is present in highly evolved fish species, such as Nile tilapia and orange-spotted grouper, whereas the tac3b gene has been lost. tac3 in fish and amphibians can encode two mature peptides, NKB and an NKB-related peptide (NKBRP), whereas there is only NKB in mammals, birds, and reptiles. NKB and NKBRP sequences are highly conserved, and sequence analysis showed that NKB and NKBRP share an identical -FXGLM motif at the C-terminus, and X is a hydrophobic or aromatic amino acid residue, which plays an important role in binding to homologous receptors.NKB exerts biological effects by activating the endogenous receptor NK3R. The NK3R receptor belongs to the G protein-coupled receptor family and has a typical seven-transmembrane structure. NK3R is encoded by the tacr3 gene. There are two tacr3 subtypes in teleosts: tacr3a and tacr3b. There was an additional gene, called tacr3a2, in the zebrafish and grass carp, and it was produced by local genome duplication of tacr3a1. The tissue distribution shows that tac3 and tacr3 are widely expressed in the central nervous system and peripheral tissues, indicating that they have essential physiological functions. The specific expression patterns vary depending on the species. They are mainly expressed in the brain, with high expression levels in the pituitary, intestine, and gonads. NKB may participate in regulating reproduction and feeding in teleosts.Currently, studies in teleosts mainly focus on reproductive and feeding regulation. Due to the existence of multiple forms of tac3 and tacr3 genes in teleosts, the action of the NKB system on reproduction control is more complex. Using different experiment methods, such as intraperitoneal injection, intramuscular injection, and incubation of pituitary cells or pituitaries, NKB affected the expression of gnrh, kiss, lhβ, and fshβ and the secretion of LH, FSH, and E2 in fish. The physiological effects varied depending on the gonadal development stages, species, sex, treatment methods, treatment time, and dose. In addition, NKB can act as an anorectic peptide to inhibit food intake and promote gastrointestinal motility. It could also affect the expression of growth-related genes. In summary, as a neurotransmitter or neuromodulator in the central nervous system and a major member of the brain-gut peptides, the NKB system plays an important role in teleosts.Tachykinins activate receptors by coupling to Gαs and Gαq proteins, transducing its signals via PKA and PKC pathways. NKB and NKBRP could activate the PKA/PKC pathway via cognate receptors in some teleosts. This could be verified because different pathway inhibitors could block the effects of NKB and NKBRP. Upon binding to NK3R, NKB induces the secretion of related neuropeptides and the expression of related genes through the AC/cAMP/PKA, PLC/IP3/PKC, and Ca2+/CaM/CaMK-Ⅱ cascades. The C-terminal motif of NKB is crucial to binding receptors; once it is changed, NKB cannot activate the downstream signaling of NK3R, indicating that the integrity of the NKB/NK3R system is essential for the normal functioning of NKB. There are many deficiencies in the research regarding the function of NKB in teleosts. The specific effects and mechanisms of regulating reproductive endocrinology remain unclear, and the functional and signaling interactions between NKB and other neuroendocrine factors such as Kiss, GnIH, and GnRH require further study. In addition, the physiological functions of NKB in fish are mainly focused on reproductive regulation, with less attention given to feeding regulation and other physiological effects.In conclusion, this review provides a summary of the research progress on the NKB system in teleosts, including the identification, tissue distribution, physiological functions, and signaling mechanisms of NKB and its receptors, to enhance the understanding of the NKB system in fish and provide a reference for future research.

Objective To investigate the effect of indoxyl sulfate (IS) on myocardial remodeling in a mouse model of myocardial infarction (MI). Methods A total of 50 adult male C57BL/6J mice were randomly divided into sham-operation group (Sham group) with 10 mice, sham operation+indoxyl sulfate group (Sham+IS group) with 10 mice, myocardial infarction group (MI group) with 15 mice, and myocardial infarction+indoxyl sulfate group (MI+IS group) with 15 mice. Left anterior descending coronary artery ligation was performed to establish a mouse model of MI, and at 24 hours after surgery, the mice in the Sham+IS group and the MI+IS group were given intraperitoneal injection of IS (100 mg/kg), while those in the Sham group and the MI group were given intraperitoneal injection of an equal volume of PBS, once a day for 28 consecutive days. The survival status of the mice in each group was recorded during this period of time. On day 30 of the experiment, echocardiography was performed to evaluate the cardiac function of mice in each group. Ultra-performance liquid chromatography was used to measure the serum concentration of IS. Masson staining was used to assess the degree of myocardial fibrosis in the infarct zone. RT-qPCR was used to measure the mRNA expression levels of α-sma and Collagen Ⅰ in myocardial tissue. Western blot was used to measure the protein expression levels of the TGF-β signaling pathway marker proteins TGF-β, p-Smad2, and p-Smad3 in myocardial tissue. Results On day 30 of the experiment, the MI+IS group had a significant reduction in the survival rate of mice compared with the MI group (χ2=5.02,P0.05). Compared with the MI group, the MI+IS group had significant increases in LVIDd and LVIDs (t=3.96,4.31,P

Myelodysplastic syndrome (MDS) is a malignant clonal disease with high heterogeneity in cytogenetics and molecular genetics, and the risk of progression to acute myeloid leukemia (AML) is extremely high. Transforming growth factor-β (TGF-β) is closely related to the pathogenesis of MDS. It is a key executor of immune homeostasis and immune tolerance, and can inhibit the expansion and function of many components of immune system. TGF-β signaling pathway can regulate hematopoietic cells and immune cells in microenvironment, inhibit their normal biological functions, and thus accelerate the progression of MDS. This study reviews regulatory effects of TGF-β signaling pathway on MDS blood cells, T lymphocytes, natural killer cells and macrophages in recent years, and provides a new perspective for the pathogenesis and treatment of MDS. [ABSTRACT FROM AUTHOR]

Acute liver failure (ALF) is one of the most critical liver diseases in clinical practice and seriously affects the life and health of Chinese people. Due to its high morbidity and mortality rates, unclear pathogenesis, and limited treatment methods, ALF has become a major problem that needs to be solved urgently in the field of liver diseases. In recent years, more and more studies have shown that endoplasmic reticulum stress is a key biological process in the progression of ALF, and the IRE1α/TRAF2/JNK pathway, as a part of endoplasmic reticulum stress signaling, plays a role in amplifying inflammatory response, promoting hepatocyte apoptosis, and inhibiting liver regeneration ability during the progression of diseases. As a traditional treasure of China, traditional Chinese medicine has become a research hotspot in search for effective prevention and treatment drugs for ALF from monomers of Chinese herbs. This article elaborates on the mechanism of action of the IRE1α/TRAF2/JNK pathway in the progression of ALF and summarizes the potential value of several monomers of Chinese herbs in regulating this pathway, such as salidroside, Fructus Broussonetiae, Fructus Psoraleae+Schisandra chinensis, baicalein, genipin, kaempferol, resveratrol, sea buckthorn polysaccharide extract, and luteol, in order to provide a reference for further research and clinical practice of ALF. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effect of sevoflurane postconditioning against cerebral ischemia/reperfusion (I/R) injury in rats and its mechanism of action. Methods A total of 80 specific pathogen-free healthy adult male Sprague-Dawley rats were selected and randomly divided into sham-operation group (S group), cerebral I/R group (I/R group), cerebral I/R+sevoflurane postconditioning group (ISP group), and cerebral I/R+sevoflurane postconditioning+nuclear factor ery-throid 2-related factor 2 (Nrf2) inhibitor group (ISPB group), with 20 rats in each group. All rats except those in the S group were used to establish a rat model of cerebral I/R injury using the suture method for occlusion of the middle cerebral artery for 2 h, followed by reperfusion for 24 h, and for the rats in the S group, threading was performed below the middle cerebral artery without ligation. The rats in the ISP group were given inhalation of 3% sevoflurane immediately after reperfusion for 30 min, and those in the ISPB group were given intraperitoneal injection of the Nrf2 inhibitor brusatol (2 mg/kg) at 30 min before ischemia in addition to the treatment in the ISP group. After successful modeling, neurological deficit score was used to eval-uate the degree of neurological impairment. Left ventricular blood samples and pathological sections of brain tissue were obtained, and 2,3,5-triphenyltetrazolium chloride staining was used to determine the percentage of cerebral infarct volume; enzyme-linked immunosorbent assay was used to measure the serum levels of inflammatory factors (interleukin-1β [IL-1β] and tumor necrosis factor-α [TNF-α]) and oxidative stress-related factors (malondialdehyde [MDA] and superoxide dismutase [SOD]); Western blotting was used to mea-sure the expression of apoptosis-related proteins (B-cell lymphoma-2 [Bcl-2], Bcl-2 related x [Bax], and Caspase-3) and Nrf2 signaling pathway-related proteins (Nrf2 and heme oxygenase-1 [HO-1]) in brain tissue; immunofluorescence assay was used to measure the expression of Nrf2 inside and outside the nucleus of brain tissue cells. Results Compared with the I/R group, the ISP group had significant reductions in neurological deficit score, the percentage of cerebral infarct volume, the serum levels of IL-1β, TNF-α, and MDA, and the levels of Bax and Caspase-3 in brain tissue (t=5.76-18.39,P

Magnetic fields are safe and used in noninvasive physical therapies. Numerous studies have confirmed that magnetic fields have good osteogenic effects and certain value for clinical application in accelerating orthodontic tooth movement, promoting bone-implant integration, promoting fracture healing and improving the effects of distraction osteogenesis. Magnetic fields are expected to become applied as effective auxiliary methods for treating oral diseases. To support the clinical application of magnetic fields, this article reviews the applications of magnetic fields in the oral cavity, the biological effects on bone cells and the molecular mechanisms through which magnetic fields regulate bone metabolism. The biological effects of magnetic fields on bone cells include promoting osteogenesis by osteoblasts and mesenchymal stem cells and inhibiting bone resorption by osteoclasts. At the molecular level, bone cells sense and respond to magnetic stimulation, and through various mechanisms, such as displacement currents, Lorentz forces, and free radical pair effects, stimuli are transformed into biologically recognizable electrical signals that activate complex downstream signaling pathways, such as the P2 purinergic receptor signaling pathway, adenosine receptor signaling pathway, transforming growth factor-β receptor signaling pathway, mammalian target of rapamycin (mTOR) pathway, and Notch pathway. In addition, magnetic parameters, which are the factors affecting the osteogenic effects of magnetic fields, are discussed. However, the mechanisms of the osteogenic effects of magnetic fields are unclear, and further studies of these mechanisms could provide effective strategies for bone regeneration and periodontal tissue regeneration. In addition, considering the target of magnetic field therapies, combination with other drugs could lead to new strategies for the treatment of oral diseases.

Extracellular vesicles (EVs), as extracellular membrane particles, play a crucial role in intercellular signaling. Research suggests that EVs may be used as biomarkers for specific organs (such as the inner ear) or as drug delivery systems. The molecules released by EVs under stress and healthy conditions are different, and these active molecules can recognize the body's disease state. Research has shown that EVs can be used to deliver drugs to structurally complex organs, such as cochlear sensory hair cells and the brain, as they can cross the blood-labyrinth and blood-brain barrier. In this review, we summarize the biological composition and biogenesis of EVs, separation techniques, characterization methods, potential therapeutic applications as drug delivery carriers, drug loading methods, and potential applications in the treatment of the inner ear within the auditory system.

Background The incidence of multiple myeloma has long been high, however, there are fewer studies on phosphatidylinositol 3-kinase (PI3K) /serine-threonine kinase (AKT) signaling pathway and M2 macrophage polarization promoting the progression of multiple myeloma. Objective To investigate the expression of M2 macrophages in patients with multiple myeloma and the mechanism of PI3K/AKT signaling pathway promoting M2 macrophage polarization. Methods Forty-eight multiple myeloma patients diagnosed in the Department of Hematology of the Affiliated Hospital of Guilin Medical University from October 2021 to April 2022 were selected as the test group, and thirty healthy volunteers (healthy donors of blood marrow transplantation) in the same period were selected as the control group. Peripheral blood was taken from the 2 group and mononuclear cells were isolated, the proportion of M2 macrophages was determined by flow cytometry. RPMI8226 cells were subcultured by cell passage, and mononuclear macrophages THP-1 cells were cultured as macrophages by phorbol ester differentiation. According to the experimental requirements, tumor cells were cultured and transfected with siRNA to silence phosphatase and tensin homolog (PTEN) and divided into three groups, including blank group, siRNA-PTEN experimental group, and siRNA control group; the supernatants of the above three groups were collected and added to the macrophage co-culture system and then divided into four groups including M0 macrophage group, tumor cell supernatant group, siRNA-PTEN supernatant group, and siRNA supernatant group. The protein expression levels of AKT, p-AKT, PI3K-p85, and p-PI3K-p85 in the blank group, siRNA-PTEN experimental group, and siRNA control group of multiple myeloma cell culture were determined by Western blot assay. The mRNA expression levels of MMP2 and MMP9 in the blank group, siRNA-PTEN experimental group and siRNA control group were determined by fluorescence quantitative polymerase chain reaction (PCR) . The expression levels of specific antibodies CD163, CD206, and F4/80 in M2 macrophages in M0 macrophage group, tumor cell supernatant group, siRNA-PTEN supernatant group, and siRNA supernatant group were determined by flow cytometry. The mRNA expression levels of arginase 1 (ARG-1) and interleukin 10 (IL-10) in M0 macrophage group, tumor cell supernatant group, siRNA-PTEN supernatant group, and siRNA supernatant group were determined by fluorescence quantitative PCR. Results The expression level of M2 macrophages was higher in the test group than that in the control group (t=0.855, P

Fetal growth restriction (FGR) is a common obstetric condition and resulting in low birth weight and reduced muscle mass in newborns after birth. This may be closely related to the regulatory mechanisms of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Studies have found that these two inflammatory factors are expressed at abnormal levels in FGR fetuses, affecting the proliferation and differentiation of myoblasts, interfering with the normal development of skeletal muscle. Moreover, TNF-α and IL-6 can activate specific signaling pathways, such as nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase (MAPK), and other signaling pathways that regulate myocyte metabolism and function. Using specific anti -inflammatory drugs or biological agents to reduce the activity of TNF-α and IL-6 may help improve the skeletal muscle development in FGR fetuses. Overall, the role of TNF-α and IL-6 in the skeletal muscle development of FGR fetuses is a multifaceted and complex process, requiring further in -depth research to clarify their specific mechanisms, aiding to the understanding of the pathophysiology of FGR, and providing new ideas for the treatment of FGR fetuses. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office 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.)

Polygonum multiflora (PM), a commonly used Chinese herbal medicine in clinical practice, has been associated with frequent reports of liver injury in recent years, and the medication safety of PM has attracted more and more attention in China and globally. This article reviews the recent research advances in the signaling pathways and mechanisms of PM in causing drug induced liver injury (DILI) and aims to provide new ideas for the proper and rational use of PM in clinical practice. The results show that PM is involved in the regulation of various signaling pathways, and it leads to the death of hepatocytes by destroying mitochondrial function, exacerbating bile acid accumulation, and inducing immune response, oxidative stress, and endoplasmic reticulum stress, thereby inducing the development and progression of DILI through multiple targets, pathways, and levels. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of kinesin family member 15（KIF15） on the proliferation of hepatocellular carcinoma （HCC） cells and its mechanism of action. Methods TCGA and GEPIA datasets were analyzed to determine the expression of KIF15 in HCC and its effect on tumor stage and survival. Quantitative real-time PCR and Western blot were used to measure the expression level of KIF15 in human-derived HCC cell lines （HepG2, Hep3B, MHCC-97H, and LM3） and human normal liver cell line L02 cultured in vitro, and Hep3B and HepG2 were selected for subsequent studies. CCK-8 assay, plate colony formation assay, and EdU staining were performed for Hep3B cells transfected with shRNA-NC or shRNA-KIF15 and HepG2 cells transfected with LV-vector or LV-KIF15 to evaluate the viability and proliferative capacity of these cells. GSEA was used to analyze the potential signaling pathways associated with KIF15 in HCC, and Western blot was used for detection. The independentsamples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results The analysis of TCGA and GEPIA datasets showed that in HCC patients, the expression of KIF15 in HCC tissue was significantly higher than that in normal tissue, and the HCC patients with high KIF15 expression tended to have a poorer prognosis. Compared with shNC-Hep3B, sh3-Hep3B showed significant reductions in the mRNA and protein levels of KIF15（P<0.05）, cell viability, clone formation number, and EdU positive rate （all P<0.05）. Compared with vector-HepG2, LV-KIF15-HepG2 showed significant increases in the mRNA and protein levels of KIF15（P<0.05）, cell viability, clone formation number, and EdU positive rate （all P< 0.05）. Subcutaneous tumor assay showed that compared with sh-NC-Hep3B, sh3-Hep3B showed reductions in tumor volume and tumor weight, as well as a significant reduction in the immunohistochemical score of Ki67 and a significant increase in the immunohistochemical score of TUNEL （P<0.05）. GSEA analysis showed that the PI3K/AKT/mTOR pathway was positively correlated with KIF15 in HCC （NES=1.59，P<0.001）. Western blot showed that LY294002 could inhibit the PI3K/AKT/mTOR pathway upregulated in LV-KIF15-HepG2, and compared with LV-KIF15-HepG2, LY294002+LV-KIF15-HepG2 showed significant reductions in cell viability, clone formation number, and EdU positive rate （all P<0.05）. Conclusion KIF15 enhances the viability and proliferative capacity of HCC cells by upregulating the PI3K/AKT/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

脑梗死是全球范围内致残率和致死率较高的疾病之一，大量研究表明，远端缺血预适应（remote ischemic preconditioning，RIPC）能够显著提高靶器官对缺血的耐受程度，减小梗死面积，改善患者预后，但目前对其在脑梗死发生发展中的作用机制研究较少。本文将从神经、体液和免疫3个方面，结合相关信号通路对RIPC在脑梗死中的作用及作用机制进行总结，并综述RIPC目前在临床缺血性脑疾病中的应用进展，以期为后续研究提供参考依据。 Abstract: Cerebral infarction is one of the diseases with high rates of disability and death worldwide, but there is still a lack of more effective treatments. Many studies showed that remote ischemic preconditioning (RIPC) can significantly improve ischemic tolerance of target organs, reduce infarct size and improve prognosis. However, its role and mechanism in the development of cerebral infarction are still little studied. This paper will summarize the role and mechanism of RIPC in cerebral infarction from the following aspects: neural, humoral, immune and related signaling pathways, and review the current research progress of RIPC in clinical cerebral ischemic diseases to provide a reference for subsequent research.

In response to nutrient limitation, Bacillus and Clostridium can form metabolically dormant spores, which are extremely resistant to a variety of environmental stresses. The ubiquitousness of spores in the environment makes it inevitable for them to enter the food processing chain. Once suitable conditions are available, spores will rapidly germinate to resume vegetative growth, thereby causing food spoilage. Since germination induces the loss of stress resistance in dormant spores, germination-inactivation strategy has been developed to mildly kill spores while maintaining food quality. Understanding the spore germination process of diverse bacterial species, the related signal transduction mechanism and the factors impacting the germination process are beneficial to develop efficient and precise strategies for inducing spore germination and raising the efficiency of inactivation, which is of great significance to the control of spores in foods. This review describes the mechanisms of the spore germination of Bacillus subtilis, Clostridium perfringens and C. difficile in terms of spore germination receptor activation and signal transduction. Moreover, inducers and inhibitors of spore germination of diverse bacterial species are also comprehensively summarized. This review provides a theoretical foundation for effectively controlling bacterial spores in foods and ensuring food quality.

Cerebral infarction is one of the diseases with high rates of disability and death worldwide, but there is still a lack of more effective treatments. Many studies showed that remote ischemic preconditioning (RIPC) can significantly improve ischemic tolerance of target organs, reduce infarct size and improve prognosis. However, its role and mechanism in the development of cerebral infarction are still little studied. This paper will summarize the role and mechanism of RIPC in cerebral infarction from the following aspects: neural, humoral, immune and related signaling pathways, and review the current research progress of RIPC in clinical cerebral ischemic diseases to provide a reference for subsequent research. [ABSTRACT FROM AUTHOR]

Insulin resistance (IR) is associated with the genesis and development of polycystic ovary syndrome (PCOS). The abnormity of insulin -related signaling pathways causes metabolism disorder, which affects follicle development and quality. In ovarian granulosa cells of PCOS, the classical pathways of insulin include phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK). The pathways related with inflammation include Toll-like receptor (TLR)/nuclear factor-κB (NF-κB), and the pathways of oxidative stress include nuclear factor-erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) and GTPase of immunity-associated protein 7 (GIMAP7)/ sonic hedgehog (SHH). There are multiple pathways related with metabolism, such as the lipid metabolism -related pathway of activating transcription factor 4 (ATF4). Therefore, clarifying the IR-related signal transduction pathway and molecular mechanism in ovarian granulosa cells of PCOS patients can supplement the knowledge of PCOS pathogenesis, and further provide new ideas for the treatment of PCOS. [ABSTRACT FROM AUTHOR]

Liver fibrosis is a key step in the progression of chronic liver diseases to liver cirrhosis and even liver cancer. In recent years， a large number of studies have shown the necessity of intervening in the process of liver fibrosis, and various anti-liver fibrosis drugs and active ingredients have been discovered. Non-coding RNAs also play an important role in the process of liver fibrosis, and searching for upstream non-coding RNAs that can regulate signaling pathways can provide new insights for anti-liver fibrosis treatment. This article introduces the process of liver fibrosis mediated by the TGF-β, Wnt/β-catenin, PI3K/ Akt/mTOR, NF-κβ, Hippo, and MAPK signaling pathways, lists the latest anti-liver fibrosis drugs or active components in each signaling pathway, and summarizes the research advances in anti-liver fibrosis targets and drugs mediated by related non-coding RNAs, so as to provide new research ideas and treatment methods for anti-liver fibrosis treatment. [ABSTRACT FROM AUTHOR]

Gallbladder carcinoma （GBC） is a type of malignant tumor with an extremely poor prognosis, and at present, surgical operation is the most effective treatment method for this disease. Unfortunately, due to a lack of typical symptoms in the early stage， most patients have progressed to the advanced stage at the time of confirmed diagnosis and lost the opportunity for radical surgery. Among the currently available adjuvant treatments, targeted therapy has higher specificity and fewer side effects and has improved the prognosis of a variety of malignancies. With reference to the latest research advances in targeted therapy for GBC, this article reviews the current research status, potential targets, and targeted medications of targeted therapy for GBC， in order to provide a reference for the clinical treatment of GBC patients. [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.)

Plant small signaling peptides（SSPs）are a class of small peptides with a protein length of less than 120 amino acids. They play an important role as novel signaling molecules in plant responses to abiotic stresses. There are over thousand kinds of SSPs in plants. Their diverse structural features, modification processes, and the binding of different receptors exert their specific functions to participate in the interactions between plants and their environment. The identification of functional genes of plant SSPs and the analysis of their regulatory mechanisms in response to abiotic stresses are of great theoretical and practical importance for enhancing plant resistance and improving plant growth. Plant SSPs mainly include four major categories: extracellular non-secretory small peptides, intracellular non-secretory small peptides, extracellular post-translational modified secretory small peptides, and extracellular cysteine-rich secretory small peptides. We briefly describe four types of plant SSPs'structure and characteristics in this review. We also elucidate their regulatory mechanisms in which SSP ligands bind to LRR-RLK receptor kinases to complete the signal transduction process and activate the expressions of downstream resistance genes. We mainly elaborate on their biological functions and their function mechanisms in response to abiotic stresses such as drought, high temperature, salinity, and nutrient deficiency. Finally, we discuss the future research directions and unresolved issues of plant SSPs. We also look forward to the development of corresponding SSPs-based growth regulators, aiming to provide new ideas for improving plant responses to environmental stress and achieving sustainable agricultural development [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the common malignant tumors of the digestive tract and seriously threatens the life of patients due to a high incidence rate, a high degree of malignancy, strong invasion and metastasis, and poor prognosis. At present, the main methods for the prevention and treatment of HCC include drugs, surgery, and interventional treatment, but all of these methods have certain adverse reactions and side effects. As an important intracellular signal transduction pathway in the human body, the JAK/STAT signaling pathway mainly exerts an anti-HCC effect by regulating cell invasion, metastasis, proliferation, growth, apoptosis, autophagy, angiogenesis, inflammation/immune response, iron metabolism, and drug resistance. Therefore, targeting the JAK/STAT signaling pathway plays an important role in the prevention and treatment of the development and progression of HCC. Traditional Chinese medicine has attracted wide attention due to its advantages of multiple targets, pathways, components, and levels in the treatment of HCC, and many cell or animal experiments on traditional Chinese medicine in the treatment of HCC have shown that the JAK/STAT signaling pathway is an important target for the prevention and treatment of HCC, with the effects of improving liver function, reducing HCC recurrence, and improving immunity. Based on this, this article analyzes the mechanism of action of the JAK/ STAT signaling pathway in HCC, as well as the intervention effect of traditional Chinese medicine monomers, traditional Chinese medicine extracts, and traditional Chinese medicine compounds on the JAK/STAT signaling pathway, in order to provide theoretical basis and reference for the prevention and treatment of HCC and the research and development of new traditional Chinese medicine drugs. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effect of remimazolam on cerebral nerves in a rat model of cerebral ischemia/reperfusion injury and its mechanism. Methods A total of 50 male Sprague-Dawley rats were randomly divided into sham-operation group (Sham group), cerebral ischemia/reperfusion group (I/R group), I/R+remimazolam (RE) group, I/R+RE+LY294002 (LY) group, and I/R+LY group. Neurological deficit score was used to evaluate the degree of neurological dysfunction. After arterial blood samples and brain tissue pathological sections were collected from the rats in each group, 2,3,5-trip-henyltetrazolium chloride staining was performed for the brain tissue sections to calculate cerebral infarct volume ratio; ELISA was used to measure the serum levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α); Western blotting was used to measure the relative expression levels of protein kinase B (AKT), phosphorylated AKT (p-AKT), nuclear factor-kappa B p65 (NF-κB p65), and phosphorylated NF-κB p65 (p-NF-κB p65) in brain tissue, and then immunofluorescence assay was used to measure the expression level of p-NF-κB p65 inside and outside the nucleus of cells in brain tissue. Results There were significant differences between these groups in cerebral infarct volume ratio, neurological deficit score, the serum levels of IL-6, IL-1β, and TNF-α, the relative expression levels of p-AKT and p-NF-κB p65, p-AKT/AKT ratio, and p-NF-κB p65/NF-κB p65 ratio (F=72.41-654.90,P

Objective To study the effect of peptide TAT-Q368-T379 intervention based on the carboxyl-terminal 375STANT379 phosphorylation site of μ opioid receptor (MOR) on the MOR downstream signaling pathway. Methods HEK-293 cells co-transfected with HA-MOR plasmids and pGloSensorTM-22F plasmids were divided into blank group (group A), DAMGO group (group B), morphine group (group C), 0.5×10-5 mol/L peptide TAT-Q368-T379 combined with morphine group (group D), 10-5 mol/L peptide TAT-Q368-T379 combined with morphine group (group E), and 2×10-5 mol/L peptide TAT-Q368-T379 combined with morphine group (group F). The GloSensor cAMP biosensor was used to measure cAMP content in each group. HEK-293 cells co-transfection with plasmids labeled with Nanoluc at the MOR-C terminal and plasmids labeled with EYFP at the β-arrestin2-N terminal were divided into blank group (group G), DAMGO group (group H), morphine group (group I), 10-5 mol/L peptide TAT-Q368-T379 combined with morphine group (group J), and 3×10-5 mol/L Cmpd101 combined with morphine group (group K). Protein interaction analysis assay was used to determine the recruitment of β-arrestin2 after MOR activation in each group. HEK-293 cells transfected with HA-MOR plasmids were divided into blank group (group L), morphine group (group M), 10-5 mol/L peptide TA-Q368-T379 combined with morphine group (group N), and 3×10-5 mol/L Cmpd101 combined with morphine group (group O). Live cell immunofluorescence staining assay was used to determine the mean fluorescence intensity of receptors in each group. Results The results of GloSensor cAMP biosensor showed that the median effective concentration (EC50) values of groups C to F were significantly different (F=13.12,P

Objective To investigate the effects of indole-2,3-dione (ISA) on the proliferation and migration of SH-SY5Y cells and the underlying mechanisms. Methods CCK-8 assay was used to assess the effect of ISA on the viability of SH-SY5Y cells, and half maximal inhibitory concentration (IC50) was calculated and used as the reference value of concentration setting in subsequent experiments. On the basis of IC50, SH-SY5Y cells were added with ISA at the final concentrations of 0, 50, 100, and 200 μmol/L (groups A, B, C, D, respectively). The effects of ISA on the proliferation, migration, apoptosis, and cell cycle of SH-SY5Y cells were determined by plate cloning, scratch assay, cell apoptosis rate detection, and PI staining flow cytometry analysis. Western blot assay was used to determine the relative expression of proteins such as Bax and Bcl2 in SH-SY5Y cells. Results The CCK-8 assay showed that the activity of SH-SY5Y cells decreased significantly with the increase in ISA concentration (F=1 632.62,P

Protein kinases regulate signaling pathways in eukaryotic cells. The phosphorylation function of kinases has attracted the attention of scientists and been deeply studied. However, some kinases are called “pseudokinases” due to missing of the key amino acids in the key motif during evolution, which leads to disruption of their phosphoryl-transfer activity. The fact that these pseudokinases are conserved across species argues that although pseudokinases have lost their phosphoryl-transfer activity, they may acquire the phosphorylation-independent functions and participate in the cellular signal transduction as well. The phosphorylation-independent functions of pseudokinases are listed as follows: 1. Directly regulating the phosphorylation activity of active kinases by binding with them; 2. Regulating the phosphorylation activity of active kinases by competitive inhibition; 3. Acting as molecular switches to perform key non-catalytic functions; 4. Acting as signaling scaffolds to assist in cell signaling; 5. Exerting catalytic functions other than phosphorylation activity. These functions have been shown to be involved in important physiological processes such as development, immunity and metabolism. Mutations or abnormal expression of pseudokinases are associated with the occurrence of various diseases such as tumors, neurological diseases, metabolic diseases and autoimmune diseases. In this article, we summarize the functions of pseudokinases in cellular signal transduction and provide a perspective for the future directions in the study of pseudokinases. [ABSTRACT FROM AUTHOR]

To investigate the protective effect of melatonin on myocardial ischemia reperfusion injury(IRI) by regulating Akt/FOXO4/BIM signaling pathway and its mechanism. Methods Myocardial IRI model was established, and cells were divided into the control group (CTRL group), the ischemia reperfusion group (IRI group), the melatonin treatment group (IRI+MEL group) and the Akt inhibitor group (IRI+MEL+MK2206 group). MTT method was used to detect the cell survival rate. The level of released LDH was measured with microplate reader. Flow cytometry was used to detect cell apoptosis. PCR method was used to detect the inflammatory gene levels of interleukin 6 (IL-6), tumor necrosis factor α (TNF- α) and monocyte chemotactic protein-1 (MCP-1). Western blot assay was used to detect the protein expression changes of p-Akt, p-FOXO4 and BIM. Results Compared with the CTRL group, the cell survival rate decreased and LDH content increased, the early stage and total apoptosis rates were increased, expression levels of IL-6, TNF-α and MCP-1 genes were increased, p-Akt protein expression decreased, and p-FOXO4 and BIM protein expression levels increased in the IRI group (P＜0.05). Compared with the IRI group, melatonin therapy increased the cell survival rate and p-Akt protein expression, decreased LDH content, cell apoptosis, IL-6, TNF- α, MCP-1 gene level and p-FOXO4 and BIM protein expression (P＜0.05). Compared with the IRI+MEL group, MK2206 partially reversed the protective effect of melatonin on IRI cardiomyocytes (P＜0.05). Conclusion Melatonin has protective effect on ischemia reperfusion injured myocardial cells, and its mechanism may be related to the regulation of Akt/FOXO4/BIM signaling pathway to reduce apoptosis and cell inflammation. [ABSTRACT FROM AUTHOR]

Embryo arrest is a common early pathological pregnancy in which is caused by defects of fertilized eggs or adverse pregnancy factors of the mother, resulting in the embryo to stop developing during pregnancy. The incidence of embryo arrest has increased year by year, becoming the most common complication of pregnancy. It may eventually lead to spontaneous abortion and missed abortion. Many factors are related to the occurrence of embryo arrest and about half of them are related to immune factors. Cytokines are a class of biologically active molecules that modulate immune response, among which inflammatory cytokines are related to inflammation. Uterine decidua and trophoblast cells can secrete a variety of inflammatory cytokines. Recent studies have shown that in the process of embryonic development, different cytokines cooperate, depend on and antagonize each other to form a cytokine network and participate in the maternal fetal interface immune response. But the exact mechanism of inducing embryo arrest is still unclear. This review focused on the relationship between inflammatory cytokines and embryo arrest and the related mechanism, in order to laying a theoretical foundation for the prevention of embryonic abortion and the development of targeted therapeutic agents. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease worldwide and can progress to nonalcoholic steatohepatitis, liver cirrhosis, and liver cancer. Mammalian target of rapamycin (mTOR) is an atypical serine/threonine protein kinase and plays an important role in the processes such as cell growth, apoptosis, autophagy, and metabolism. This article elaborates on the role of the mTOR complex 1 (mTORC1) signaling pathway in cell metabolism, growth, and differentiation during in the onset of NAFLD and further proposes the value and potential of the mTORC1 pathway in the research on therapeutic drugs for NAFLD. [ABSTRACT FROM AUTHOR]

The molecular mechanism of tobacco growth inhibition induced by boron stress was not clear yet. The tobacco ' K326' at 8 leaves stage as experimental materials were cultured in Hoagland solutions with 0, 0.05, 1.00, 2.00, 3.00 mmol⋅L-1 boron, respectively. After 4 weeks of treatment, the contents of total sugar, protein, chlorophyll, H2O2, boron and the antioxidant enzyme activities in tobacco leaves were detected. The transcriptome sequencing technology was used to analyze the differentially expressed genes (DEGs) and the significantly enriched metabolic pathways responding to boron stress in tobacco leaves. The results showed that, the higher the boron content, the more significant inhibition were found on the growth of tobacco plants. 2.00 mmol⋅L-1 boron treatment significantly inhibited the growth of roots, stems, and leaves of tobacco; and significantly inhibit carbohydrate metabolism, increase H2O2 contents, and enhance peroxidase (POD) activity in leaves. Compared with tobacco treated with normal Hoagland solution (0.05 mmol⋅L-1 boron), 389 DEGs that responded to 2.00 mmol⋅L-1 boron stress specifically were enriched in sugar metabolism, lipid metabolism, hormone signaling, and plant disease resistance signaling pathways. It was found that the boron stress affected carbon and lipid metabolism in tobacco leaves, and inhibited tobacco growth by altering hormone signaling pathways. These results provided some basis for further understanding the mechanism of response to boron stress in tobacco. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality 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.)

The incidence rate of alcoholic liver disease (ALD) is increasing year by year China, and there is a gradual increase in disease burden among Chinese people. Oxidative stress response in hepatocytes is an important pathogenic mechanism of ALD. The nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway is an important endogenous anti-oxidative stress pathway in the body, and Nrf2 is activated in response to oxidative stress and exerts its transcriptional activity to induce high HO-1 expression. HO-1 is an important oxidative stress response protein and plays a role in anti-inflammation, anti- oxidation, and cell apoptosis regulation together with heme hydrolysis products (bilirubin, carbon monoxide, and iron). This article reviews the research advances in the role of the Nrf2/HO-1 signaling pathway in ALD in recent years, so as to find a theoretical basis for the development and progression of ALD and an entry point for treatment. [ABSTRACT FROM AUTHOR]

The mechanical force caused by elevated blood pressure plays a decisive role in vascular differentiation and development, the maintenance of normal vascular structure and function, and the process of vascular lesions. Abnormal elevation of blood lipid and/or blood glucose synergistically accelerate mechanical force-initiated vascular remodeling and the occurrence and development of diseases. Mechanical forces can nonspecifically activate all transmembrane protein molecules in vascular cells, leading to simultaneous activation of intracellular multi-signal channel molecules (secondary effector molecules). The upstream multi-pathway molecular signals converge on the node molecules of signal network and then diverge to the downstream pathway molecules, and finally start more signaling pathway activation, and amplify the signal cascades. Then, a series of pathophysiological changes such as cell differentiation, migration, inflammation, phenotypic changes, calcification, proliferation, and apoptosis occur. Finally, the structural and functional changes of blood vessels, such as atherosclerosis, become the main cause of death and disability caused by cardiovascular and cerebrovascular diseases. This paper reviews the research progress from this research group and international peers, that is, vascular remodeling is closely related to the effect of mechanical force generated by elevated blood pressure on vascular smooth muscle cells. [ABSTRACT FROM AUTHOR]

Objective To investigate the role and mechanism of action of Scabiosa atropurea in inhibiting the proliferation of hepatic stellate cells using cell experiment. Methods A total of 20 Wistar rats were randomly divided into control group and administration group, with 10 rats in each group. The rats in the control group were given normal saline by gavage, and those in the administration group were given Scabiosa atropurea by gavage to prepare drug-containing serum. HSC-T6 cells were incubated with the serum from the control group（10%) or the low-, middle-, and high-dose serum containing Scabiosa atropurea（10%, 15%, and 20%, respectively). MTT assay was used to observe the effect of different drug concentrations on cells in different periods of time; flow cytometry was used to measure cell apoptosis; qRT-PCR and Western blot were used to measure the mRNA and protein expression levels of fibrosis markers（α-SMA, collagen Ⅰ) and PI3K/Akt signaling pathway-related factors in hepatic stellate cells（HSCs). A one-way analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results Compared with the control group, the low-, middle-, and high-dose serum containing Scabiosa atropurea groups had a significant reduction in the OD value of cells（all P＜0.05) and a significant increase in the overall apoptosis rate of cells（all P＜0.05). The results of qRT-PCR showed that compared with the control group, the low-, middle-, and high-dose serum containing Scabiosa atropurea groups had significant reductions in the mRNA expression levels of α-SMA, collagen Ⅰ, PI3K, and Akt and a significant increase in the mRNA expression level of PTEN（all P＜0.05); Western blot showed that compared with the control group, the low-, middle-, and high-dose serum containing Scabiosa atropurea groups had significant reductions in the protein expression levels of α-SMA, collagen Ⅰ, PI3K, Akt, and p-Akt and a significant increase in the protein expression level of PTEN（all P＜0.05). Conclusion The Mongolian medicine Scabiosa atropurea can inhibit the proliferation of HSC-T6 cells and promote their apoptosis, possibly by regulating fibrosis markers and the PI3K/Akt signaling pathway to exert an anti-liver fibrosis effect. [ABSTRACT FROM AUTHOR]

Copyright of Acta Prataculturae Sinica is the property of Acta Prataculturae Sinica Editorial Office 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 expression and role of the Sonic Hedgehog（Shh） signaling pathway in intestinal mucosal barrier injury in rats with severe acute pancreatitis（SAP）. Methods A total of 48 Sprague-Dawley rats were divided into sham-operation group（Sham group）, SAP model group（SAP group）, SAP+Shh signaling pathway-specific agonist purmorphamine group（PUR+SAP group）, and SAP+Shh signaling pathway-specific antagonist cyclopamine group（CYC+SAP group） using a random number table, with 12 rats in each group, and each group was further divided into 12-hour and 24-hour subgroups, with 6 rats in each subgroup. Rats were given retrograde injection of 5% sodium taurocholate into the pancreatic and bile ducts to establish a model of SAP, and rats in the intervention groups were given intraperitoneal injection of 0.69 mg/kg purmorphamine and 0.69 mg/kg cyclopamine before modeling. Related samples were collected at 12 and 24 hours after modeling. HE staining was used to observe the pathological changes of the pancreas and the ileum; ELISA was used to measure the serum levels of amylase, lipase, diamine oxidase（DAO）, and endotoxin-core antibody（EndoCAb）; the TUNEL method was used to observe the apoptosis of intestinal epithelial cells; Western blot was used to measure the expression levels of Shh, Ptch1, and Gli1 in ileal tissue. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups; the Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between multiple groups and further comparison between two groups. Results Compared with the Sham group, the SAP group had significant increases in the pathological scores of pancreatic and ileum tissue, the serum levels of lipase, amylase, DAO, and EndoCAb, the apoptosis of intestinal epithelial cells, and the protein expression levels of Shh, Ptch1, and Gli1 in ileal tissue（all P＜0.05）. Compared with the SAP group, the PUR+SAP group had significantly alleviated pathological injury and dysfunction of the pancreas and intestine, a significant reduction in the apoptosis of intestinal epithelial cells, and significant increases in the protein expression levels of Shh, Ptch1, and Gli1 in ileal tissue（all P＜0.05）. Compared with the SAP group, the CYC+SAP group had significant aggravation of the pathological injury and dysfunction of the pancreas and intestine, a significant increase in the apoptosis of intestinal epithelial cells, and significant reductions in the protein expression levels of Shh, Ptch1, and Gli1 in ileal tissue（all P＜0.05）. Conclusion The Shh signaling pathway may be involved in intestinal mucosal barrier injury in SAP and exerts a protective effect. [ABSTRACT FROM AUTHOR]

Plant endogenous polypeptides are composed of natural amino acids in different composition and arrangement from the precursor proteins cut into mature polypeptides, which play biological function in development and stress response after secreted outside the cells and recognized by their receptors. The plant endogenous polypeptide family PIP (PAMP induced secret peptide) /PIP-Like (PIPL) contains SGPS and GxGH motifs recognized by receptor like kinase 7 (RLK7), and plays important roles in pathogen resistance, virus resistance, salt resistance and development. Here, we review the signal transduction pathways of PIP/PIPL family polypeptides in the process of resistance to stress and development, discuss important unsolved scientific issues, and prospect possible applications, aiming to provide the references on further researches on PIP/PIPL. [ABSTRACT FROM AUTHOR]

As a chronic liver inflammation disease caused by the lack of immune tolerance, autoimmune hepatitis is regulated by various signaling pathways, such as the NF-κB/NLRP3 pathway, the SIRT1/Nrf2/HO-1 pathway, the Hippo-YAP/TAZ pathway, the JAK/STAT pathway, the PI3K/Akt pathway, and the TRAF6/JNK pathway. These pathways can play a role against autoimmune hepatitis by participating in the processes including the proliferation and apoptosis of cytokines, immune response, and oxidative stress. In view of the problems of suboptimal response, obvious adverse reactions, and high recurrence rate in the clinical application of hormones and immune preparations for the treatment of autoimmune hepatitis, this article summarizes the research articles on autoimmune hepatitis-related signaling pathways and the mechanism of effective constituents（glycosides, terpenoids, flavonoids, quinones, and phenols） in traditional Chinese medicine intervening against the disease process of autoimmune hepatitis through the above signaling pathways, in order to provide a theoretical basis for scientific and effective utilization of effective constituents in traditional Chinese medicine to develop anti-autoimmune hepatitis drugs. [ABSTRACT FROM AUTHOR]

Pre-eclampsia is one of the common complications of pregnancy and is an important cause of maternal and perinatal mortality. The disordered functions of placental trophoblast cells are closely associated with the development of preeclampsia. Inadequate invasion of placental extravillous trophoblast cells and abnormal spiral artery remodelling are dominant pathologic mechanisms in pre-eclampsia. The PI3K/Akt (phosphatdylinositol-3 kinase/protein kinase B) signalling pathway plays a significant role in regulating proliferation, survival, apoptosis, migration, and invasion of trophoblast cells. MicroRNAs (miRNAs), long non-coding RNAs and circular RNAs belonging to non-coding RNAs (ncRNA) have multi-level regulatory roles on genes and influence the functions of trophoblast cells by regulating the PI3K/Akt signalling pathway, thus contributing to the occurrence and development of pre -eclampsia. This review introduces the recent advances of ncRNAs related to PI3K/Akt signalling pathway in pre -eclampsia in an effort to provide a reference for exploring and discovering key molecules in the pathogenesis of pre-eclampsia. [ABSTRACT FROM AUTHOR]

Stimulator of interferon genes (STING) signaling pathway is a natural immune pathway, which can be activated by bacterial or viral DNA fragments in cytoplasm to promote type I interferon production through a series of downstream signaling pathways. It is a central part of the human anti-tumor immunity. Previous studies have found that STING expression was up-regulated in some human papilloma virus (HPV)-positive tumor tissues, and high expression of STING was associated with a better prognosis of tumor patients. We could observed remarkable regression of tumor when injecting STING agonists into tumor tissues. However, other studies believe that the immune escape of HPV could interfere with STING signaling pathways and other natural immune pathways at the transcriptional level, promote epigenetic silencing and autophagy degradation of STING, thus creating an immunosuppressive microenvironment of tumor and promoting tumor growth. Herein we will systematically elaborate the role of STING signaling pathway in HPV-positive malignant tumors and analyze the potential therapeutic value of STING agonists in HPV-positive tumors. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression levels of scf and c-kit under the regulation of Dahuang Lingxian prescription and the possible mechanism of its effect on gallbladder dynamics, and to provide a theoretical basis for Dahuang Lingxian prescription in preventing the development and recurrence of cholesterol gallstone. Methods A total of 45 specific pathogen-free healthy male guinea pigs were randomly divided into normal group, model group, and traditional Chinese medicine (TCM) group. The guinea pigs in the normal group were fed with normal diet, and those in the model group and the TCM group were fed with high-fat lithogenic diet. After 8 weeks of feeding, 5 guinea pigs were randomly selected from each group, and successful modeling was determined if gallstone was observed with the naked eye in more than 4 guinea pigs. After successful modeling, the guinea pigs in the TCM group were given Dahuang Lingxian prescription by gavage, and those in the model group were given an equal volume of normal saline by gavage. After 8 consecutive weeks of administration by gavage, gallbladder tissue samples were collected, and HE staining was used to observe the pathological changes of gallbladder tissue; Western blot was used to measure the expression level of tumor necrosis factor-α (TNF-α) in gallbladder tissue; immunohistochemistry was used to measure the protein expression levels of scf and c-kit in gallbladder smooth muscle tissue. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups, and the least significant difference multiple comparison method was used for further comparison between two groups. Results HE staining showed marked inflammation of gallbladder tissue in the model group, and compared with the model group, the TCM group had a significantly lower degree of inflammation. Western blot showed that the model group had the highest expression level of TNF-α in gallbladder tissue, followed by the TCM group and the normal group (P < 0.05); immunohistochemistry showed that compared with the model group, the normal group and the TCM group had significantly higher protein expression levels of scf and c-kit in gallbladder smooth muscle tissue (P < 0.05). Conclusion Dahuang Lingxian prescription can enhance the dynamic function of the gallbladder, possibly by upregulating the scf/c-kit signaling pathway in interstitial cells of Cajal in gallbladder. [ABSTRACT FROM AUTHOR]

Cell signaling pathway refers to the process that extracellular factors combine with membrane receptors and nuclear receptors to lead to the interaction and biochemical process of a series of proteins in cells so that the genes to be expressed in cells begin to form various biological effects.Hepatic stellate cell（HSC） is an important protective barrier of human liver.For example, when liver injury factors invade in the external environment, HSC will be activated immediately and quickly change from the original static state to the activated state.However, in the process of activation, the body participates in a large number of cells and cytokines, which interact and transform each other, resulting in further aggravation of fibrosis in hepatocytes.Many previous experimental studies have shown that the action mechanism of anti-hepatic fibrosis drugs is multi-level cross regulation, which is a very complex network system.It can inhibit the activation and proliferation of HSC from a variety of signal pathways, so as to inhibit hepatic fibrosis, and inhibit the overall process of liver cirrhosis.This paper summarized seven signaling pathways involved in the study of HSC activation.With the help of the study of HSC activation and proliferation, this paper explored the effect and treatment process of hepatic fibrosis caused by HSC activation and proliferation under the action of signaling pathway. [ABSTRACT FROM AUTHOR]

Pre-eclampsia (PE) is a common clinical idiopathic pregnancy disease. Its condition changes dynamically, and its clinical manifestations are diversified. The etiology and mechanism have not been fully clarified so far. The main research results show that it is closely related to genetic factors, immune factors, nutritional factors and environmental factors. Recent studies have shown that the mammalian target of rapamycin (mTOR) signal pathway is involved in the regulation of placental trophoblast and vascular endothelial cell activity by regulating cell proliferation, invasion, migration and apoptosis, and insulin signal initiates downstream molecules to regulate cell metabolism by activating mTOR signal pathway, which leads to maternal vascular endothelial injury, damaged uterine spiral arteriole remodeling and abnormal inflammatory immune response, and so on, and participates in the occurrence of PE. The purpose of this review is to explore the correlation between mTOR signaling pathway and the pathogenesis of PE, and to provide theoretical basis for pathophysiological research and disease treatment of PE. [ABSTRACT FROM AUTHOR]

Copyright of Acta Agronomica Sinica is the property of Crop Science Society of China 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 Chinese Institute of Food Science & Technology is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office 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.)

The regulatory Tcells (Treg) and helper Tcells 17 (Th17) play an important role in regulation of the tumor microenvironment in hepatocellular carcinoma (HCC) because Treg/Thl 7 imbalance was associated with HCC cell invasion and progression. Moreover, the suppressor of cytokine signaling 1 ( SOCSl), a negative regulator of the Janus kinase ( JAK )/ signal transducers and activators of transcription (STAT) pathway, regulates Treg and Th 17 proliferation and differentiation. This review summarized and discussed the recent advancement and progress in control of the Treg/Th17 balance in HCC and the immunity - related mechanisms in HCC development and progression, i. e., the SOCSl structure and functions, SOCSl role in regulation of Treg/Thl 7 balance in HCC, and future research direction of the field . [ABSTRACT FROM AUTHOR]

Hepatic fibrosis is a common pathological stage of many chronic liver diseases. Activation of hepatic stellate cells is considered as a key event in the progression of hepatic fibrosis. The pathogenesis of liver fibrosis is modulated by various cytokines involved in several signal pathways, including NF - KB, TGF - J3/Smad, Wnt/J3 - catenin, Hedgehog etc. With the rapid development of modern pharmacology and biotechnology, the underlying molecular mechanism of anti - liver fibrosis of active components from traditional Chinese medicine has been further elucidated. This article summarizes scientific outcomes of signal pathways involved in liver fibrosis and how active components of Chinese herbal medicines exhibit anti - liver fibrosis effects, aiming to provide a potential drug candidate as a treatment for liver fibrosis and to open up a new research field of therapeutics for liver fibrosis. [ABSTRACT FROM AUTHOR]