Search

BACKGROUND: Oyster polypeptide (OP) is a mixture of oligopeptides extracted from oysters through enzyme lysis, separation, and purification. It is associated with immunomodulatory effects, but the underlying mechanisms are not known. This study therefore combined proton nuclear magnetic resonance (1H‐NMR) urinary metabolomics and 16S rRNA gene sequencing of the gut microbiome to determine the immunoprotective mechanisms of OP in rats subjected to cyclophosphamide‐induced immunosuppression. RESULTS: Oyster polypeptide restored the body weight and the structure of spleen and thymus in rats with cyclophosphamide‐induced immunosuppression. It upregulated the levels of white blood cells (WBCs), hemoglobin (HGB), platelets (PLT), red blood cells (RBCs), immunoglobulin G (IgG), immunoglobulin M (IgM), cytokines such as interleukin‑6 (IL‐6) and tumor necrosis factor‐α (TNF‐α), and increased the numbers of CD3+ and CD4+ T cells in the immunosuppressed rats. The 1H‐NMR metabolomics results showed that OP significantly reversed the levels of ten metabolites in urine, including 2‐oxoglutarate, citrate, dimethylamine, taurine, N‐phenylacetylglycine, alanine, betaine, creatinine, uracil, and benzoate. The 16S rRNA gene sequencing results showed that OP restored the gut microbiome homeostasis by increasing the abundance of beneficial bacteria and reducing the abundance of pathogenic bacteria. Finally, a combination of metabolomics and microbiomics found that the metabolism of taurine and hypotaurine, and the metabolism of alanine, aspartate, and glutamate were disturbed, but these metabolic pathways were restored by OP. CONCLUSION: This study demonstrated that OP had immunoprotective effects in rats with cyclophosphamide‐induced immunosuppression by restoring key metabolic pathways and the gut microbiome homeostasis. Our findings provide a framework for further research into the immunoregulatory mechanisms of OP and its potential use in drugs and nutritional supplements. © 2024 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Aging is a known independent risk factor for several cardiovascular diseases. Here, we evaluated potential effects and possible mechanisms through which alginate oligosaccharides (AOS) affect hydrogen peroxide (H2O2)-induced senescence in H9C2 cardiomyocytes. A series of AOS molecules, including oligoM, oligoG, M-5, and G-5, were investigated. AOS significantly decreased SA-β-gal and DAPI-stained positive cells, downregulated p53 and p21 (aging-related markers) expression, and eventually protected H9C2 cells from H2O2-induced senescence. AOS decreased reactive oxygen species and malondialdehyde production, recovered mitochondrial function, and alleviated the oxidative stress state by regulating PGC-1α and NADPH oxidase subunit expression. Furthermore, AOS treatment restored the expression of antioxidant enzymes in senescent H9C2 cells. Thus, our results show in vitro evidence that AOS alleviate senescence in H9C2 cells by regulating the redox state; thus, AOS may be an effective therapeutic agent that could protect against cardiomyocyte senescence. [ABSTRACT FROM AUTHOR]

Introduction: Postpartum endometritis is a prevalent reproductive disorder in bovines, leading to a prolonged open period, infertility, and other complications. While Lactobacillus strains can mitigate these conditions by reducing uterine inflammation, their effectiveness is limited due to a lack of direct anti microbial action and extended treatment duration. This study aimed to construct a recombinant Lactobacillus johnsonii strain expressing bovine Granulocytemacrophage colony-stimulating factor (GM-CSF) to evaluate its potential in reducing postpartum uterine inflammation. Methods: The recombinant Lactobacillus johnsonii strain was engineered to express bovine GM-CSF and administered to pregnant mice via vaginal perfusion. Postpartum endometritis was induced using E. coli infection, and the protective effects of the engineered strain were assessed. Inflammatory markers (IL-6, IL-1β, TNF-α), myeloperoxidase (MPO) activity, and nitric oxide (NO) concentration were measured. Histological examination was performed to evaluate uterine morphology and pathological damage. Results: The recombinant L. johnsonii strain expressing GM-CSF significantly reduced inflammation levels induced by E. coli infection in the uterus. This reduction was evidenced by decreased expression of IL-6, IL-1β, TNF-α, as well as reduced MPO activity and NO concentration. Histological examination revealed improved uterine morphology and reduced pathological damage in mice treated with the recombinant GM-CSF strain. Crucially, the recombinant strain also exerts beneficial effects on bovine endometritis by reducing levels of inflammatory cytokines, suggesting a beneficial effect on clinical bovine endometritis. Conclusion: The recombinant Lactobacillus johnsonii expressing GM-CSF demonstrated protective effects against postpartum endometritis in bovines by reducing inflammatory cytokines. The findings indicate the potential clinical application of this engineered strain in preventing postpartum uterine inflammation, offering a novel and effective protective option for related disorders and improving bovine reproductive efficiency. [ABSTRACT FROM AUTHOR]

Fermented mare's milk (koumiss), a traditional Central Asian dairy product derived from fermented mare's milk, is renowned for its unique sour taste and texture. It has long been consumed by nomadic tribes for its nutritional and medicinal benefits. This study aimed to comprehensively analyze the protective effects of koumiss against alcohol-induced harm across behavioral, hematological, gastrointestinal, hepatic, and reproductive dimensions using a mouse model. Optimal intoxicating doses of alcohol and koumiss doses were determined, and their effects were explored through sleep tests and blood indicator measurements. Pretreatment with koumiss delayed inebriation, accelerated sobering, and reduced mortality in mice, mitigating alcohol's impact on blood ethanol levels and various physiological parameters. Histopathological and molecular analyses further confirmed koumiss's protective role against alcohol-induced damage in the liver, stomach, small intestine, and reproductive system. Transcriptomic studies on reproductive damage indicated that koumiss exerts its benefits by influencing mitochondrial and ribosomal functions and also shows promise in mitigating alcohol's effects on the reproductive system. In summary, koumiss emerges as a potential natural agent for protection against alcohol-induced harm, opening avenues for future research in this field. [ABSTRACT FROM AUTHOR]

Dehydrins proteins accumulate and play important protective roles in most plants during abiotic stresses. The objective of this study was to characterize a YSK2-type dehydrin gene, WDHN2, isolated from Triticum aestivum previously. In this work, wheat dehydrin WDHN2 was expressed in Escherichia coli and purified by immobilized metal affinity chromatography, which exhibited as a single band by sodium dodecyl sulfonate polyacrylamide gel electrophoresis and western blotting. We show that WDHN2 is capable of alleviating lactate dehydrogenase inactivation from heat and desiccation in vitro enzyme activity protection assay. In vivo assay of Escherichia coli viability demonstrates the enhancement of cell survival by the overexpression of WDHN2. The protein aggregation prevention assay explores that WDHN2 has a broad protective effect on the cellular proteome. The results show that WDHN2 is mainly accumulated in the nucleus and cytosol, suggesting that this dehydrin may exert its function in both cellular compartments. Our data suggest that WDHN2 acts as a chaperone molecular in vivo. [ABSTRACT FROM AUTHOR]

Background: Maternal anxiety, depression, and stress during and after pregnancy are negatively associated with child cognitive development. However, the contribution of positive maternal experiences, such as social support, to child cognitive development has received less attention. Furthermore, how maternal experience of social support during specific developmental periods impacts child cognitive development is largely unknown. Methods: Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 5784) and the Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction study (PREDO; n = 420), we investigated the associations between maternal perceived social support during and after pregnancy and child's general cognitive ability at 8 years of age, assessed with the Wechsler Intelligence Scale for Children (WISC). Bayesian relevant life course modeling was used to investigate timing effects of maternal social support on child cognitive ability. Results: In both cohorts, higher maternal perceived social support during pregnancy was associated with higher performance on the WISC, independent of sociodemographic factors and concurrent maternal symptoms of depression and anxiety. In ALSPAC, pregnancy emerged as a sensitive period for the effects of perceived social support on child cognitive ability, with a stronger effect of social support during pregnancy than after pregnancy on child cognitive ability. Conclusions: Our findings, supported from two prospective longitudinal cohorts, suggest a distinct role of maternal perceived social support during pregnancy for cognitive development in children. Our study suggests that interventions aimed at increasing maternal social support during pregnancy may be an important strategy for promoting maternal and child well-being. [ABSTRACT FROM AUTHOR]

HPSE2, the gene‐encoding heparanase 2 (Hpa2), is mutated in urofacial syndrome (UFS), a rare autosomal recessive congenital disease attributed to peripheral neuropathy. Hpa2 lacks intrinsic heparan sulfate (HS)‐degrading activity, the hallmark of heparanase (Hpa1), yet it exhibits a high affinity toward HS, thereby inhibiting Hpa1 enzymatic activity. Hpa2 regulates selected genes that promote normal differentiation, tissue homeostasis, and endoplasmic reticulum (ER) stress, resulting in antitumor, antiangiogenic, and anti‐inflammatory effects. Importantly, stress conditions induce the expression of Hpa2, thus establishing a feedback loop, where Hpa2 enhances ER stress which, in turn, induces Hpa2 expression. In most cases, cancer patients who retain high levels of Hpa2 survive longer than patients bearing Hpa2‐low tumors. Experimentally, overexpression of Hpa2 attenuates the growth of tumor xenografts, whereas Hpa2 gene silencing results in aggressive tumors. Studies applying conditional Hpa2 knockout (cHpa2‐KO) mice revealed an essential involvement of Hpa2 contributed by the host in protecting against cancer and inflammation. This was best reflected by the distorted morphology of the Hpa2‐null pancreas, including massive infiltration of immune cells, acinar to adipocyte trans‐differentiation, and acinar to ductal metaplasia. Moreover, orthotopic inoculation of pancreatic ductal adenocarcinoma (PDAC) cells into the pancreas of Hpa2‐null vs. wild‐type mice yielded tumors that were by far more aggressive. Likewise, intravenous inoculation of cancer cells into cHpa2‐KO mice resulted in a dramatically increased lung colonization reflecting the involvement of Hpa2 in restricting the formation of a premetastatic niche. Elucidating Hpa2 structure–activity‐relationships is expected to support the development of Hpa2‐based therapies against cancer and inflammation. [ABSTRACT FROM AUTHOR]

Testicular torsion is a critical urologic condition for which testicular detorsion surgery is considered irreplaceable as well as the golden method of reversal. However, the surgical treatment is equivalent to a blood reperfusion process, and no specific drugs are available to treat blood reperfusion injuries. Salidroside (SAL) is one of the main effective substances in rhodiola, which has been shown to have antioxidant and antiapoptosis activities. This study was designed to determine whether SAL exerted a protective effect on testicular ischemia-reperfusion (I/R) injury. In this study, the I/R injury model of the testes and reoxygenation (OGD/R) model were used for verification, and SAL was administered at doses of 100 mg/kg and 0.05 mmol/L, respectively. After the experiments, the testicular tissue and TM4 Sertoli cells were collected for histopathologic and biochemical analyses. The results revealed that SAL improves the structure of testicular tissue and regulates the oxidation-antioxidation system. To further understand the molecular mechanisms of SAL in treating testicular I/R injuries, transcriptomics and metabonomics analyses were integrated. The results show that the Nfr2/HO-1/GPX4/ferroptosis signaling pathway is enriched significantly, indicating that it may be the main regulatory pathway for SAL in the treatment of testicular I/R injuries. Thereafter, transfection with Nrf2 plasmid-liposome was used to reverse verify that the Nfr2/HO-1/GPX4/ferroptosis signaling pathway was the main pathway for SAL anti-testicular I/R injury treatment. Thus, it is suggested that SAL can protect against testicular I/R injuries by regulating the Nfr2/HO-1/GPX4 signaling pathway to inhibit ferroptosis and that SAL may be a potential drug for the treatment of testicular I/R injuries. [ABSTRACT FROM AUTHOR]

Objectives: The protective effects and related mechanisms of Jing-Si herbal tea (JSHT) were investigated in cellular damage mediated by pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor-a, on normal human lung fibroblast by multiomic platform analysis. Materials and Methods: The in silico high-throughput target was analyzed using pharmacophore models by BIOVIA Discovery Studio 2022 with ingenuity pathway analysis software. To assess cell viability, the study utilized the MTT assay technique. In addition, the IncuCyte S3 ZOOM System was implemented for the continuous monitoring of cell confluence of JSHT-treated cytokine-injured HEL 299 cells. Cytokine concentrations were determined using a Quantibody Human Inflammation Array. Gene expression and signaling pathways were determined using next-generation sequencing. Results: In silico high-throughput target analysis of JSHT revealed ingenuity in canonical pathways and their networks. Glucocorticoid receptor signaling is a potential signaling of JSHT. The results revealed protective effects against the inflammatory cytokines on JSHT-treated HEL 299 cells. Transcriptome and network analyses revealed that induction of helper T lymphocytes, TNFSF12, NFKB1-mediated relaxin signaling, and G-protein coupled receptor signaling play important roles in immune regulatory on JSHT-treated cytokine-injured HEL 299 cells. Conclusion: The findings from our research indicate that JSHT holds promise as a therapeutic agent, potentially offering advantageous outcomes in treating virus infections through various mechanisms. Furthermore, the primary bioactive components in JSHT justify extended research in antiviral drug development, especially in the context of addressing coronavirus. [ABSTRACT FROM AUTHOR]

Abstract Background Liver fibrosis is an irreversible liver destruction. Apigenin (API) has different pharmacological properties as anticancer, anti-inflammatory, and antioxidant; however, API hepatoprotective and therapeutic effects are not often studied. This study assesses protective and therapeutic API effects on hepatic injuries produced by thioacetamide (TAA) in rats. Methods Forty-nine rats were sorted into seven groups (7 in each): negative control (G1), positive control (G2, TAA), API group (G3), TAA+API group (G4), TAA+SL group (G5), API+TAA group (G6), and SL+TAA group (G7). API and SL effects on TAA-induced hepatotoxicity were examined by determined body weights, liver weights, complete blood count picture (white blood cells, red blood cells, hemoglobin, hematocrit, and platelets counts), liver function tests (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transferase, alkaline phosphatase, total proteins, albumin, and globulin), and oxidative stress markers (malonaldehyde, catalase, superoxide dismutase, and reduced glutathione) in serum and liver histological was assessed. Results TAA decreased red blood cells, platelets, hemoglobin content, and hematocrit (p

ABSTRACTThe uric acid (UA) induced damage influences human health and deserves attention. The purpose of this study was to investigate the protective effects of Skipjack trypsin hydrolysate (STH) and its Maillard product (STH-M) and the segmentation of STH-M (STH-M-S) against UA-induced HK-2 cells. The CCK8 assay was used to detect cell viability and flow cytometry was performed to check cell apoptosis and cell cycle and the functional mechanism was analyzed via transcriptome. The results showed STH-M-S could significantly improve the cell viability and inhibit cell apoptosis. Meanwhile, STH-M-S could influence the membrane and protein binding and regulate metabolic-related and immune-related pathways to deal with UA stress. Functional genes contained NEBL, KCNJ16, ABCA12, CLDN2, FLRT3, PRODH, KLHL14, VEPH1, HPGD (down regulated) and FOXL1, SCG5 (up regulated). Collectively, our results suggested that STH-M-S can alleviate cell injury induced by UA. STH-M-S could be an alternative to be applied for the treatment of hyperuricemia.

Background: Liver fibrosis is an irreversible liver destruction. Apigenin (API) has different pharmacological properties as anticancer, anti-inflammatory, and antioxidant; however, API hepatoprotective and therapeutic effects are not often studied. This study assesses protective and therapeutic API effects on hepatic injuries produced by thioacetamide (TAA) in rats. Methods: Forty-nine rats were sorted into seven groups (7 in each): negative control (G1), positive control (G2, TAA), API group (G3), TAA+API group (G4), TAA+SL group (G5), API+TAA group (G6), and SL+TAA group (G7). API and SL effects on TAA-induced hepatotoxicity were examined by determined body weights, liver weights, complete blood count picture (white blood cells, red blood cells, hemoglobin, hematocrit, and platelets counts), liver function tests (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transferase, alkaline phosphatase, total proteins, albumin, and globulin), and oxidative stress markers (malonaldehyde, catalase, superoxide dismutase, and reduced glutathione) in serum and liver histological was assessed. Results: TAA decreased red blood cells, platelets, hemoglobin content, and hematocrit (p <0.001) and increased white blood cells count (p <0.001) versus control. Serum values of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transferase, alkaline phosphatase, and malondialdehyde significantly elevated (p <0.001); meanwhile, total protein, albumin, globulin, catalase, superoxide dismutase, and glutathione S transferase decline (p <0.001) versus negative control. Hepatic structure of TAA group revealed fibrosis and hepatocyte destruction. Therapeutic or protective treating TAA-rats with API or SL ameliorate hematological values, liver functions, oxidative stress, and histological alterations especially therapeutic effects on hematological changes, liver function tests, and oxidative stress markers. Conclusions: Apigenin had therapeutic and protective effects on liver fibrosis due to its antioxidant activity with therapeutic better than protective effects. [ABSTRACT FROM AUTHOR]

In recent years, Artocarpus heterophyllus Lam. (jackfruit) polysaccharides (namely JFP-Ps) have attracted much attention due to their multiple biological activities. This study aimed to explore the protective effects and the underlying mechanisms of JFP-Ps on cyclophosphamide (Cp)-induced liver damage. The protective effect of JFP-Ps was evaluated using HE staining, antioxidant testing, enzyme-linked immunosorbent assay (ELISA), real-time quantitative polymerase chain reaction (RT-qPCR), Western blot and ultra-performance liquid chromatography equipped with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS) metabolomics analysis. The results showed that Cp caused pathological liver damage, activated oxidative stress and downregulated cytokine expression, while JFP-Ps treatment was found to exert antioxidant effects and play immune regulatory roles through mitogen-activated protein kinase/nuclear factor-κB (MAPK/NF-κB) related inflammation and cell apoptosis pathways to protect the Cp-induced liver injury. Metabolomic results showed that the liver-protective effects of JFP-Ps were mainly related to aminoacyl transfer ribonucleic acid (tRNA) biosynthesis, sphingolipid metabolism, purine metabolism and the citrate cycle. These results indicate that JFP-Ps have great potential application in alleviating liver injury. [ABSTRACT FROM AUTHOR]

Fermented mare’s milk (koumiss), a traditional Central Asian dairy product derived from fermented mare’s milk, is renowned for its unique sour taste and texture. It has long been consumed by nomadic tribes for its nutritional and medicinal benefits. This study aimed to comprehensively analyze the protective effects of koumiss against alcohol-induced harm across behavioral, hematological, gastrointestinal, hepatic, and reproductive dimensions using a mouse model. Optimal intoxicating doses of alcohol and koumiss doses were determined, and their effects were explored through sleep tests and blood indicator measurements. Pretreatment with koumiss delayed inebriation, accelerated sobering, and reduced mortality in mice, mitigating alcohol’s impact on blood ethanol levels and various physiological parameters. Histopathological and molecular analyses further confirmed koumiss’s protective role against alcohol-induced damage in the liver, stomach, small intestine, and reproductive system. Transcriptomic studies on reproductive damage indicated that koumiss exerts its benefits by influencing mitochondrial and ribosomal functions and also shows promise in mitigating alcohol’s effects on the reproductive system. In summary, koumiss emerges as a potential natural agent for protection against alcohol-induced harm, opening avenues for future research in this field.

Microalgal cells are the major contributors of extracellular polymeric substances (EPS) in the marine environment, which could be influenced by exogenous pollutants exposure. As the most dominant brominated flame retardant worldwide, studies on the influence of tetrabromobisphenol A (TBBPA) on microalgal cells and EPS production are rare. Therefore, we systemically investigated the physiological-biochemical responses of the marine diatom Thalassiosira pseudonana to TBBPA exposure and the roles of EPS. Our results indicated that the half effective concentrations (EC50) of TBBPA on T. pseudonana were 1.67–3.22 mg L−1 from 24 to 96 h; Photosynthetic damage, cellular materials increase, cellular oxidative stress and cell death were found under the toxicity of TBBPA, in which cellular materials increase and oxidative stress were positively correlated with the increase of EPS contents. The increase of soluble and bound EPS contents, protein/carbohydrate ratios together with the EPS addition assays indicated the protective effects of EPS to alleviate the toxicity of TBBPA. Increased microalgal EPS secretions and protein/carbohydrate ratios also happened under the environmental TBBPA concentration (2 μg L−1), which might accelerate the organic matters aggregation process especially in coastal areas. [ABSTRACT FROM AUTHOR]

Introduction: Prosocial behavior during childhood has been associated with numerous positive developmental and behavioral outcomes in adolescence and adulthood. Prosocial behavior, which includes cooperation and helping others, develops within a bioecological context. Considering it through such a lens enhances the understanding of the roles of different bioecological factors in its development. Methods: Using data from a longitudinal study of adopted children and children reared with their biological parents, this paper examined if positive aspects of a child's bioecological system at age 7 predict prosocial behavior in early adolescence (age 11), and whether these bioecological factors could offset risk due to biological family psychopathology and/or maternal prenatal substance use. The analyses incorporated variables from different levels of Bronfenbrenner's bioecological model (the individual, microsystem, exosystem, and macrosystem) and examined the promotive, and potentially protective, effect of each contextual factor, while also considering their interplay with biological family psychopathology and prenatal substance use. Results: Results from linear regression models indicated that the microsystem variable of parental warmth at age 7 had a promotive effect on age 11 prosocial behavior. Further, in addition to its main effect, parental warmth was protective against maternal substance use during pregnancy when children were raised with their biological parent (s). Household type (biological family) and biological family internalizing psychopathology were the only other significant predictors in the model, with each associated with lower prosocial behavior at age 11. Discussion: Study results extend prior work on the benefits of parental warmth on child outcomes by employing a strength-based, bioecological approach to the development of prosocial behavior during early adolescence and examining "for whom" the effects of parental warmth are most protective. [ABSTRACT FROM AUTHOR]

Zika virus (ZIKV) infection during pregnancy can result in severe birth defects, such as microcephaly, as well as a range of other related health complications. Heparin, a clinical-grade anticoagulant, is shown to protect neural progenitor cells from death following ZIKV infection. Although heparin can be safely used during pregnancy, it retains off-target anticoagulant effects if directly employed against ZIKV infection. In this study, we investigated the effects of chemically modified heparin derivatives with reduced anticoagulant activities. These derivatives were used as experimental probes to explore the structure–activity relationships. Precursor fractions of porcine heparin, obtained during the manufacture of conventional pharmaceutical heparin with decreased anticoagulant activities, were also explored. Interestingly, these modified heparin derivatives and precursor fractions not only prevented cell death but also inhibited the ZIKV replication of infected neural progenitor cells grown as neurospheres. These effects were observed regardless of the specific sulfation position or overall charge. Furthermore, the combination of heparin with Sofosbuvir, an antiviral licensed for the treatment of hepatitis C (HCV) that also belongs to the same Flaviviridae family as ZIKV, showed a synergistic effect. This suggested that a combination therapy approach involving heparin precursors and Sofosbuvir could be a potential strategy for the prevention or treatment of ZIKV infections. [ABSTRACT FROM AUTHOR]

There is a growing demand for the consumption of medicinal mushrooms and their products. Ganoderma lucidum and Cordyceps militaris are two important medicinal mushrooms with significant pharmacological activities. In this study, we aim to develop a preparation of the extracts of these two mushrooms, and investigate its composition, antioxidant activities, and protective effects against oxidative damage. Liquid chromatography equipped with quadrupole time-of-flight mass spectrometry (LC-QTOF MS) was employed to analyze the chemical profiles of the mixture. A total of 94 compounds were identified as belonging to phenolic acids, flavonoids, triterpenes, and nucleosides. In addition, HPLC-DAD was used to quantify major compounds. Ferulic and cinnamic acids were predominant in the phenolic acid groups, with corresponding concentrations of 0.41 and 0.29 mg/g. The concentration of ganoderic acid A was 0.08 mg/g, and the contents of adenosine and cordycepin were 0.53 and 0.14 mg/g, respectively. The mixture could scavenge free radicals and reduce ferric ions in vitro. The preparation also showed nontoxic but proliferative effects on human fibroblast cells. In addition, it could protect fibroblasts against oxidative stress, reducing 21–22% of cell death in the presence of H2O2. These findings provide more information on the applications of medicinal mushrooms in the functional food and pharmaceutical industries.

Alzheimer’s disease (AD) is a chronic, neurodegenerative disorder that affects the central nervous system and is found predominantly in elderly populations. As amyloid b protein (Ab) is one of the key players responsible for the pathogenesis of AD, we sought to investigate the protective effects of fisetin in an Ab1-42-induced rat model of AD. In this model, the protective effects of fisetin on learning and memory impairment induced by Ab1-42 were determined via the Morris water maze and passive avoidance test. Furthermore, the antioxidant activity, anti-inflammation, and apoptosis effect of fisetin were investigated using biochemical and immunohistochemical methods. The results showed that intragastric (i.g.) administration of fisetin (100, 50, and 25 mg/kg) improved previous learning and memory impairments in Ab1-42-treated rats. Hippocampal tissue from these fisetin-treated rats revealed that the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) were markedly enhanced, and that the levels of malondialdehyde (MDA) and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were significantly reduced. Meanwhile, fisetin also significantly attenuated Ab1-42-induced cholinergic dysfunction such as elevated the activity of choline acetyltransferase (ChAT) and reduced the activity of acetylcholine esterase (AChE). In addition, hippocampal tissue obtained from fisetin-treated rats revealed a reversal of Ab1-42-induced effects on apoptotic pathway protein (caspase-3) expression and inflammatory response of glial fibrillary acidic protein (GFAP). This indicated that the amount of degenerating hippocampal neurons with apoptotic features was dramatically reduced after treatment with fisetin. Collectively, these findings suggest that fisetin has potential as a treatment agent for Alzheimer’s disease and that its effects occur through several mechanisms, including inhibition of oxidative stress, adjustments to previous cholinergic dysfunction, anti-inflammatory actions, and decreased apoptotic activity.

Recent research has provided evidence that metal oxide nanoparticles (NPs) have the potential to traverse the placental barrier, potentially endangering the health of both pregnant individuals and the developing fetus. The function of oxidative stress is of utmost importance in the pathophysiology of poor pregnancy outcomes. The therapeutic potential of solanesol in mitigating pregnancy complications is attributed to its robust antioxidant activity. The objective of this work was to inspect the preventative effects of solanesol on the detrimental effects generated by CuO and NiO NPs in human placental cells (BeWo). It was noticed that the exposure of BeWo cells to solanesol at concentrations ranging from 1 to 100 µg/ml for a duration of 24 h did not result in any harmful effects. However, the presence of CuO and NiO NPs led to a dose-dependent decrease in cell viability when exposed to dosages of 5 to 200 µg/ml for 24 h. It is noteworthy that solanesol significantly reduced the cytotoxicity that CuO and NiO NPs generated in BeWo cells. The data on apoptosis also demonstrated that CuO and NiO NPs have effect on the expression of the apoptotic gene caspase-3 and the decline of mitochondrial membrane potential. However, this effect was effectively reversed when solanesol was administered in combination with NPs. The findings of the mechanistic investigation indicate that the CuO and NiO NPs induced oxidative stress was notably negated when solanesol was concurrently treated. This paper presents novel findings indicating that the toxicity generated by CuO and NiO NPs in human placental cells was significantly alleviated by solanesol. Further work is necessary to explore the pharmacological potential of solanesol against nanoparticle-generated pregnancy problems.

Momordica charantia polysaccharide (MCP) is a potential drug for the prevention and alleviation of diabetes mellitus (DM) and diabetic retinopathy (DR). This study aimed to investigate the potential protective effects of MCP on early-stage DR and explore the underlying mechanisms. The model group (DM group) and treatment group (D+H group) were established by inducing type 1 DM using a single dose of streptozotocin (STZ) at 60 mg/kg. After modeling, the D+H group was orally administered a 500 mg/kg dose of MCP solution once daily for 12 weeks. Monitoring of systemic indicators (FBG, body weight, general condition) and retinal tissue inflammation and apoptosis (HE staining, IL-6, MCP-1, TNF-α, VEGF, NF-κB, Caspase-3) in this study demonstrated that MCP intervention alleviated both DM and DR. MCP improved the body weight and general condition of DM rats by reducing FBG levels. It also enhanced the anti-inflammatory and anti-apoptotic capabilities of retinal neurons and microvessels by modulating the actions of cytokines, thereby further regulating the inflammation and apoptosis of retinal neurons and microvessels. The underlying mechanisms may be associated with the downregulation of NF-κB and Caspase-3 pathway protein expression, as well as the downregulation of mRNA expression of NF-κB and Caspase-3 pathway genes. Further research is needed to elucidate the potential mechanisms underlying the protective effects of MCP on DR. MCP may emerge as a selective medication for the prevention and alleviation of DM and a novel natural medicine for the prevention and alleviation of DR.

Ischemia-reperfusion (I/R) injury refers to a new injury caused by reperfusion after the restoration of ischemic tissue or organ blood supply. Salvianic acid A (danshensu) is a primary active ingredient extracted from Salvia miltiorrhiza. It has a protective function against I/R injury in the cardiovascular system, brain, liver, kidney, gastrointestinal tract, and other organs. This article reviews evidence of the protective effects of Salvianic acid A and its potential mechanisms of action in organ I/R injury protection. The aim of this review is to investigate the role of Salvianic acid A in the treatment of I/R injury, providing a reference resource that could facilitate subsequent studies.

Dasatinib (DASA) is a novel tyrosine kinase inhibitor, approved for leukemia treatment. However, the long-term use of DASA induces several complications, especially liver damage. On the other hand, Naringenin (NGN) is a potent antioxidant and anti-inflammatory agent which is known to exert protective effects in several liver disease animal models. Yet, the effect of NGN on DASA-induced hepatotoxicity has not been examined. This study investigated the hepatoprotective effects of NGN against DASA-induced acute liver injury, using a mouse model. The mice were given NGN (50, 100, and 200 mg/kg po) or saline for 7 days, followed by DASA on the eighth day (25 mg/kg p.o.). DASA treatment alone was found to cause overexpression of proinflammatory cytokines, such as interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and malonyl aldehyde (MDA), whereas attenuation of antioxidant genes including superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione peroxidase (GPx). Interestingly, a pretreatment with NGN + DASA resulted in minimizing the proinflammatory mediators and restoring the levels of antioxidant genes. In addition, there was evidence of necro-inflammatory changes in histopathological findings in the liver samples after DASA administration which remarkably reduced with NGN + DASA. Thus, this study revealed that NGN could minimize the hepatotoxicity induced by DASA by providing anti-inflammatory and antioxidant protection. [ABSTRACT FROM AUTHOR]

Acetaminophen (APAP), widely recognized for its analgesic and antipyretic properties, poses a risk of renal toxicity in cases of overdose. Traditional herbal remedies are frequently employed to counteract drug-induced renal damage. This study focuses on black shallot, an innovative food product derived from Allium ascalonicum, a plant highly valued in traditional Vietnamese medicine. The aim is to explore the protective effects of black shallot ethanol extract (BSEE) against APAP-induced nephrotoxicity in mice. BSEE was orally administered at various doses (200, 250, and 300 mg/kg) in combination with APAP (3 g/kg). N-acetylcysteine (NAC) (50 mg/kg) served as the reference drug, while saline (10 mL/kg) functioned as the negative control. Evaluations encompassed renal histology, serum and urine renal function tests, antioxidant enzyme concentrations (SOD, CAT, and GPx), lipid peroxidation, and anti-inflammatory cytokines (TNF-α, IL-1β, and IL-6). The findings indicated significant alterations in total protein, albumin, BUN, and serum/urine CRE concentrations (P < 0.05), coupled with a decrease in malondialdehyde (MDA) levels (P < 0.05) and inflammatory cytokines TNF-α, IL-1β, and IL-6 (P < 0.05). Remarkable elevations were observed in antioxidant enzyme concentrations, including renal catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) (P < 0.05). The macroscopic and microscopic structures of the kidneys exhibited significant improvement. Consequently, BSEE effectively safeguards against APAP-induced renal damage, as evidenced by enhanced renal structure, reduced inflammation, and biochemical modulation, highlighting its potential therapeutic application in preventing APAP-induced nephrotoxicity [ABSTRACT FROM AUTHOR]

Disturbances in the gut microbiota and its derived metabolites are closely related to the occurrence and development of hepatic steatosis. The white kidney bean (WKB), as an excellent source of protein, dietary fiber, and phytochemicals, has recently received widespread attention and might exhibit beneficial effects on a high-fat diet (HFD)-induced hepatic steatosis via targeting gut microbiota and its metabolites. The results indicated that HFD, when supplemented with WKB for 12 weeks, could potently reduce obesity symptoms, serum lipid profiles, and glucose, as well as improve the insulin resistance and liver function markers in mice, thereby alleviating hepatic steatosis. An integrated fecal microbiome and metabolomics analysis further demonstrated that WKB was able to normalize HFD-induced gut dysbiosis in mice, thereby mediating the alterations of a wide range of metabolites. Particularly, WKB remarkably increased the relative abundance of probiotics (Akkermansiaceae, Bifidobacteriaceae, and norank_f_Muribaculaceae) and inhibited the growth of hazardous bacteria (Mucispirillum, Enterorhabdus, and Dubosiella) in diet-induced hepatic steatosis mice. Moreover, the significant differential metabolites altered by WKB were annotated in lipid metabolism, which could ameliorate hepatic steatosis via regulating glycerophospholipid metabolism. This study elucidated the role of WKB from the perspective of microbiome and metabolomics in preventing nonalcoholic fatty liver disease, which provides new insights for its application in functional foods. [ABSTRACT FROM AUTHOR]

In recent years, Artocarpus heterophyllus Lam. (jackfruit) polysaccharides (namely JFP-Ps) have attracted much attention due to their multiple biological activities. This study aimed to explore the protective effects and the underlying mechanisms of JFP-Ps on cyclophosphamide (Cp)-induced liver damage. The protective effect of JFP-Ps was evaluated using HE staining, antioxidant testing, enzyme-linked immunosorbent assay (ELISA), real-time quantitative polymerase chain reaction (RT-qPCR), Western blot and ultra-performance liquid chromatography equipped with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS) metabolomics analysis. The results showed that Cp caused pathological liver damage, activated oxidative stress and downregulated cytokine expression, while JFP-Ps treatment was found to exert antioxidant effects and play immune regulatory roles through mitogen-activated protein kinase/nuclear factor-κB (MAPK/NF-κB) related inflammation and cell apoptosis pathways to protect the Cp-induced liver injury. Metabolomic results showed that the liver-protective effects of JFP-Ps were mainly related to aminoacyl transfer ribonucleic acid (tRNA) biosynthesis, sphingolipid metabolism, purine metabolism and the citrate cycle. These results indicate that JFP-Ps have great potential application in alleviating liver injury.

Nanogels are attractive drug delivery systems that provide high loading capacity for drug molecules, improve their stability, and increase cellular uptake. Natural antioxidants, especially polyphenols such as resveratrol, are distinguished by low aqueous solubility, which hinders therapeutic activity. Thus, in the present study, resveratrol was incorporated into nanogel particles, aiming to improve its protective effects in vitro. The nanogel was prepared from natural substances via esterification of citric acid and pentane-1,2,5-triol. High encapsulation efficiency (94.5%) was achieved by applying the solvent evaporation method. Dynamic light scattering, atomic force microscopy, and transmission electron microscopy revealed that the resveratrol-loaded nanogel particles were spherical in shape with nanoscopic dimensions (220 nm). In vitro release tests showed that a complete release of resveratrol was achieved for 24 h, whereas at the same time the non-encapsulated drug was poorly dissolved. The protective effect of the encapsulated resveratrol against oxidative stress in fibroblast and neuroblastoma cells was significantly stronger compared to the non-encapsulated drug. Similarly, the protection in a model of iron/ascorbic acid-induced lipid peroxidation on rat liver and brain microsomes was higher with the encapsulated resveratrol. In conclusion, embedding resveratrol in this newly developed nanogel improved its biopharmaceutical properties and protective effects in oxidative stress models. [ABSTRACT FROM AUTHOR]

(1) Background: Numerous meta-analyses have shown that a high intake of dietary fiber plays a protective role in preventing the development of various types of cancer. However, previous studies have been limited by focusing on a single type of dietary fiber and variations in outcome measures, which may not be effectively applied to provide dietary guidance for the general population. (2) Object: We summarized the meta-analysis of dietary fiber and cancer, and provided references for residents to prevent cancer. (3) Methods: Systematic search of relevant meta-analyses on the association between dietary fiber and cancer occurrence in PubMed, Web of Science and other databases was conducted from the time of database construction to February 2023. The method logical and evidence quality assessments were performed by applying the criteria in the "A Measurement Tool to Assess Systematic Reviews-2" (AMSTAR2) scale and the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) Expert Report, respectively. (4) Results: Our analysis included 11 meta-analyses, and the AMSTAR 2 assessment revealed that the overall methodological quality was suboptimal, with two key items lacking sufficient information. Nonetheless, our findings indicate that a high intake of dietary fiber is associated with a reduced risk of several types of cancer, including esophageal, gastric, colon, rectal, colorectal adenoma, breast, endometrial, ovarian, renal cell, prostate, and pancreatic cancers. The majority of these associations were supported by a "probable" level of evidence. (5) Conclusions: Dietary fiber intake has different protective effects on different cancers. [ABSTRACT FROM AUTHOR]

Four new phenolic glycosides lepidiumosides A–D (1–4) were isolated from the water extract of the seeds of Lepidium apetalum Willd. Their structures were determined by extensive spectroscopic (UV, IR, HR-ESI-MS, 1D and 2D NMR) analyses. In addition, these compounds were evaluated for their protective effects impaired by H2O2 in H9c2 cells, suggesting that compounds 1–4 exhibited protective effects against H2O2-induced cardiotoxicity. [ABSTRACT FROM AUTHOR]

The present research aimed to assess the protective effects of purslane polyphenols on rabbit meat myofibrillar protein (MP) under malondialdehyde (MDA)‐induced oxidation. The major polyphenols in purslane extract were analyzed by ultrahigh performance liquid chromatography‐quadrupole time‐of‐flight mass spectrometry (UPLC‐QTOF‐MS). To analyze the protective mechanism of purslane polyphenol monomers on MP in the oxidation system, we determined the retained MDA content in the suspension and analyzed the structure and nuclear magnetic resonance (NMR) of MP. The UPLC‐QTOF‐MS identification analysis indicated that purslane polyphenols mainly contained chlorogenic acid, caffeic acid, ferulic acid, rutin, kaempferol, and quercetin. Polyphenols in purslane can prevent MDA from binding to MP effectively. Chlorogenic acid showed the best inhibitory effect, and the retention content of MDA decreased to 54.79%, which was significantly lower than those of other groups. Purslane polyphenols had protective effects on sulfhydryl groups, free amino groups, intrinsic tryptophan fluorescence, α‐helix structure, and morphology of MP. Moreover, the carbonyl contents, increase in surface hydrophobicity, and random coil contents of MP were reduced. In addition, the NMR results indicated that polyphenols inhibited the oxidation of protein induced by MDA through competitive inhibition. Practical Application: This study showed the efficiency of purslane polyphenol monomers in protecting the structure and function of myofibrillar protein under malondialdehyde‐induced oxidative stress and their potential to preserve the nutritional value of foods rich in proteins and lipids. [ABSTRACT FROM AUTHOR]

Alzheimer’s disease (AD) is a chronic, neurodegenerative disorder that affects the central nervous system and is found predominantly in elderly populations. As amyloid β protein (Aβ) is one of the key players responsible for the pathogenesis of AD, we sought to investigate the protective effects of fisetin in an Aβ1-42-induced rat model of AD. In this model, the protective effects of fisetin on learning and memory impairment induced by Aβ1-42 were determined via the Morris water maze and passive avoidance test. Furthermore, the antioxidant activity, anti-inflammation, and apoptosis effect of fisetin were investigated using biochemical and immunohistochemical methods. The results showed that intragastric (i.g.) administration of fisetin (100, 50, and 25 mg/kg) improved previous learning and memory impairments in Aβ1-42-treated rats. Hippocampal tissue from these fisetin-treated rats revealed that the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) were markedly enhanced, and that the levels of malondialdehyde (MDA) and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were significantly reduced. Meanwhile, fisetin also significantly attenuated Aβ1-42- induced cholinergic dysfunction such as elevated the activity of choline acetyltransferase (ChAT) and reduced the activity of acetylcholine esterase (AChE). In addition, hippocampal tissue obtained from fisetin-treated rats revealed a reversal of Aβ1-42-induced effects on apoptotic pathway protein (caspase-3) expression and inflammatory response of glial fibrillary acidic protein (GFAP). This indicated that the amount of degenerating hippocampal neurons with apoptotic features was dramatically reduced after treatment with fisetin. Collectively, these findings suggest that fisetin has potential as a treatment agent for Alzheimer’s disease and that its effects occur through several mechanisms, including inhibition of oxidative stress, adjustments to previous cholinergic dysfunction, anti-inflammatory actions, and decreased apoptotic activity. [ABSTRACT FROM AUTHOR]

Chlorogenic acid (CGA) is a polyphenol that is present in coffee beans, many vegetables, and fruits. Since CGA has been reported to exert antioxidant and anti-inflammatory effects, it is expected to protect against periodontitis. In the present study, we used a ligature-induced experimental periodontitis model and investigated the beneficial effects of CGA against alveolar bone resorption caused by experimental periodontitis. To examine the inhibitory effects of CGA on bone loss, a ligature was wrapped around the maxillary right second molar, and CGA was intraperitoneally injected once a day for 2 weeks. In another experiment to investigate the restorative effects of CGA on bone loss, a ligature was wrapped around the maxillary right second molar for 2 weeks, it was then removed, and CGA was intraperitoneally injected once a day for 2 weeks. At the end of the experiments, the maxillae were removed, and CT images were taken. Alveolar bone loss was measured as the distance from the cement–enamel junction to the alveolar crest. The statistical analysis was performed using GraphPad Prism6 (Dunn's multiple comparison test). The results revealed that the ratio of the buccal alveolar bone loss (vs. the bone loss on the nonligated side) induced by ligation was significantly decreased by the administration of CGA (5 mg/kg) for 2 weeks. Moreover, the bone loss ratio on the buccal and palatal sides after 2 weeks of ligation was significantly decreased by the 2-week administration of CGA (5 mg/kg). The present results revealed that CGA exerted preventive effects against alveolar bone loss caused by experimental periodontitis. [ABSTRACT FROM AUTHOR]

To determine the composition and protective effect on Raw 264.7 cells of polysaccharide from Pseudostellaria heterophylla as a traditional Chinese medicinal, the main active ingredient-Pseudostellaria heterophylla polysaccharide (PHP) was extracted by water, precipitated by ethanol, and purified by anion exchange column chromatography. Gel permeation chromatography (GPC) and high performance liquid chromatography (HPLC) were used to determine molecular weight and monosaccharide composition of PHP. Ultraviolet spectroscopy (UV) and Fourier transform infrared spectroscopy (FT-IR) were used for primary structural characterization of PHP. Furthermore, the Raw 264.7 cell model was used to explore protective effect of PHP on Raw 264.7 cells induced by LPS. The results showed that the yield of crude polysaccharide of Pseudostellaria heterophylla was 8.23%, and the polysaccharide content was 51.47%. After purification by DEAE-52 column chromatography, the polysaccharide content increased to 80.52%, and the molecular weight distribution was between 500 to 92×103 Da. The monosaccharide components of PHP include glucose, galactose, arabinose, mannose and glucuronic acid. Cell experiments showed that the safe dose of PHP was 80~640 µg/mL and could increase the survival rate of cells induced by lipopolysaccharide (LPS). At a dose of 640 µg/mL, the survival rate increased by 7.21%, and it was found that PHP could improve the morphology of Raw 264.7 cells. In summary, in this study the polysaccharides from Pseudostellaria heterophylla were purified, the structure of PHP was characterized, and it was preliminarily confirmed that PHP had potential protective effect on LPS-induced damage to Raw 264.7 cells. This laid the foundation for the follow-up exploration of functional activity, structure-effect and dose-effect of PHP.

Doxorubicin (DOX) and vincristine (VC) are anti-cancer drugs commonly used for lymphoma in veterinary and human medicine. However, there are several side effects caused by these drugs. In this study, the protective effects of sonicated Bordetella bronchiseptica bacterin (sBb) on dendritic cells (DCs) damaged by two anti-cancer drugs were investigated. DCs play important roles in the innate and adaptive immunity of hosts, especially activating T cells that can suppress tumor growth. The metabolic activity of DCs significantly increased after the treatment with sBb compared to that of control DCs. In addition, there was a marked change in mitochondrial integrity between DOX-treated DC and DOX + sBb-treated DCs. Flow cytometric analysis also demonstrated that sBb upregulated the expression of the surface markers of DCs, particularly CD54. In mixed lymphocyte responses, sBb significantly increased the antigen-presenting capability of DCs. In particular, sBb increased the capability of control DCs by approximately 150% and that of VC-treated DCs by 221%. These results suggest that sBb can be used as a potential immunostimulatory agent to protect DCs from anti-cancer drug-induced damage and provide fundamental information about using a combination of DCs and vincristine in immunotherapy.

Background: Several cellular and animal studies have suggested that lipoxin A4 (LXA4) has a protective effect on type 2 diabetes mellitus (T2DM) development. However, little is known about whether LXA4 influences T2DM development at the population level. Methods: We included 2755 non-diabetic participants from a cohort study in China who were followed for about seven years. Cox proportional hazards modelwas used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) for the association between LXA4 and incident T2DM. Mediation models were used to examine how serum lipids as mediators impact the association between LXA4 and T2DM. Results: In total, 172 newly diagnosed T2DM cases were identified. Multivariateadjusted HR for T2DM in the fourth compared with the first quartile of LXA4 was 0.62 (95% CI: 0.40-0.96). When used the optimal cutoff value determined by the receiver operating characteristic curve, the results showed participants with LXA4 > 2.84 ng/mL had a decreased T2DM risk compared to those with LXA4 ≤ 2.84 ng/mL (HR: 0.63, 95% CI: 0.45-0.89). The effect of LXA4 on incident T2DM was significantly modified by gender (P-interaction = 0.024) and family history of diabetes (P-interaction = 0.025). Additionally, the association between LXA4 and incident T2DM was partially suppressed by the TyG and TG/HDL-c ratio, with a suppression proportion of 22.2% and 16.0%, respectively. Conclusions: Higher LXA4 levels are significantly associated with a lower risk of T2DM development. The present findings would be helpful in understanding the effect of LXA4 on T2DM development at the population level. [ABSTRACT FROM AUTHOR]

Background/Aim: Gastric acid reflux into the esophagus can cause irritation and inflammation of the esophagus and progress to reflux esophagitis (RE). Vitamin D3 (VitD3) has anti-inflammatory effects and plays an important regulatory role in adaptive and innate immunity. We hypothesized that VitD3 may play a protective role in RE. Materials and Methods: Seventy male Sprague-Dawley rats were used, and acute RE (n=35) or chronic RE (n=35) were surgically induced. The effects of different doses of VitD3 on morphological changes and alteration of pro-inflammatory cytokine levels were examined in the rat models. Western blot analysis was performed to determine protein expression levels of IL-1ß, IL-6, and IL-8 in esophageal tissues. Serum levels of VitD3 and calcium were determined using enzyme-linked immunosorbent assays. Results: The protein expression of proinflammatory cytokines IL-1ß, IL-6, and IL-8 was found significantly increased in RE. VitD3 treatment significantly reduced the levels of these pro-inflammatory cytokines in both the low-dose and high-dose VitD3 groups compared to control groups in acute RE, but not chronic RE. Macrographic and histopathological examination revealed various degrees of esophageal impairment in rats following surgical induction of acute or chronic RE in rats. These impairments were not improved by VitD3. Morphological grading of esophageal mucosa showed no significant differences between acute and chronic RE. Elevated serum levels of calcium were observed after VitD3 treatment. Conclusion: IL-1ß, IL-6, and IL-8 levels were significantly elevated in RE. The abnormal increase in these important pro-inflammatory cytokines was suppressed by VitD3 in the rat models of acute RE. These novel findings suggest a potential protective role of VitD3 in early-stage RE. [ABSTRACT FROM AUTHOR]

Abstract The objective of the present study was to explore the protective effects of the curcumin/cyclodextrin polymer (CUR/CDP) inclusion complex on hydrogen peroxide (H2O2)‐induced LO2 cells damage. In this study, a H2O2‐induced cells oxidative injury model was established to test the protective effects of the CUR/CDP inclusion complex. The cell viability of cells was detected by the thiazolyl blue tetrazolium bromide (MTT) assay. The extracellular lactate dehydrogenase (LDH) activity, catalase (CAT) activity, and malondialdehyde (MDA) level were detected by assay kits. The cellular reactive oxygen species (ROS) level was detected using the dichlorodihydrofluorescein (DCF) fluorescence assay. Western blotting analysis was conducted to assess the changes of phosphorylated‐p53 and caspase‐3. The results showed that 700 μM H2O2‐treated LO2 cells for 3 h resulted in a significant decrease of cell viability to 53.00 ± 1.68%, which established the cell oxidative injury model. Cells treated with H2O2 led to a significant increase of extracellular LDH activity, MDA content, and ROS level, and decreased CAT activity. Treatment with CUR/CDP significantly reversed the changes of the above indicators. Moreover, CUR/CDP treatment at 20 and 40 μg/ml inhibited H2O2‐induced increase in phosphorylated‐p53 and caspase‐3 expression, indicating that CUR/CDP suppressed cell apoptosis to alleviate liver injury. The results of those studies demonstrated that CUR/CDP had a protective effect on the oxidative damage of LO2 cells, and it could be developed as a new type of natural liver protection product to apply in the prevention of liver injury.

Abstract Background With the widespread of Coronavirus Disease 2019 pandemic, in spite of the newly emerging vaccines, mutated strains remain a great obstacle to supportive and preventive measures. Coronavirus 19 survivors continue to face great danger of contacting the disease again. As long as no specific treatment has yet to be approved, a great percentage of patients experience real complications, including among others, lung fibrosis. High oxygen inhalation especially for prolonged periods is per se destructive to the lungs. Nevertheless, oxygen remains the first line support for such patients. In the present study we aimed at investigating the role of amniotic fluid-mesenchymal stem cells in preventing versus treating the hyperoxia-induced lung fibrosis in rats. Methods The study was conducted on adult albino rats; 5 pregnant female rats were used as amniotic fluid donors, and 64 male rats were randomly divided into two groups: Control group; where 10 rats were kept in normal atmospheric air then sacrificed after 2 months, and hyperoxia-induced lung fibrosis group, where 54 rats were exposed to hyperoxia (100% oxygen for 6 h/day) in air-tight glass chambers for 1 month, then randomly divided into the following 5 subgroups: Hyperoxia group, cell-free media-treated group, stem cells-prophylactic group, stem cells-treated group and untreated group. Isolation, culture and proliferation of stem cells were done till passage 3. Pulmonary function tests, histological examination of lung tissue under light and electron microscopes, biochemical assessment of oxidative stress, IL-6 and Rho-A levels, and statistical analysis of data were performed. F-test (ANOVA) was used for normally distributed quantitative variables, to compare between more than two groups, and Post Hoc test (Tukey) for pairwise comparisons. Results Labelled amniotic fluid-mesenchymal stem cells homed to lung tissue. Stem cells administration in the stem cells-prophylactic group succeeded to maintain pulmonary functions near the normal values with no significant difference between their values and those of the control group. Moreover, histological examination of lung tissues showed that stem cells-prophylactic group were completely protected while stem cells-treated group still showed various degrees of tissue injury, namely; thickened interalveolar septa, atelectasis and interstitial pneumonia. Biochemical studies after stem cells injection also showed decreased levels of RhoA and IL-6 in the prophylactic group and to a lesser extent in the treated group, in addition to increased total antioxidant capacity and decreased malondialdehyde in the stem cells-injected groups. Conclusions Amniotic fluid-mesenchymal stem cells showed promising protective and therapeutic results against hyperoxia-induced lung fibrosis as evaluated physiologically, histologically and biochemically.

Porcine epidemic diarrhea virus (PEDV) mainly infects the intestinal epithelial cells of pigs, causing porcine epidemic diarrhea (PED). In particular, the virus causes severe diarrhea, dehydration, and death in neonatal piglets. Maternal immunity effectively protects neonatal piglets from PEDV infection; however, maternal antibodies can only prevent PEDV attachment and entry into target cells, but have no effects on intracellular viruses. Intracellular antibodies targeting virus-encoded proteins are effective in preventing viral infection. We previously identified four single chain variable fragments (scFvs), ZW1-16, ZW3-21, ZW1-41, and ZW4-16, which specifically targeted the PEDV N protein and significantly inhibited PEDV replication and up-regulated interferon-λ1 (IFN-λ1) expression in host cells. In our current study, the four scFvs were subcloned into replication-defective adenovirus vectors to generate recombinant adenoviruses rAdV-ZW1-16, rAdV-ZW3-21, rAdV-ZW1-41, and rAdV-ZW4-16. ScFvs were successfully expressed in Human Embryonic Kidney 293 (HEK293) cells and intestinal porcine epithelial cell line J2 (IPEC-J2) and were biosafe for piglets as indicated by body temperature and weight, scFv excretion in feces, IFN-γ and interleukin-4 (IL-4) expression in jejunum, and pathological changes in porcine tissue after oral administration. Western blotting, immunofluorescence, and immunohistochemical analyses showed that scFvs were expressed in porcine jejunum. The prophylactic effects of rAdV-ZW, a cocktail of the four rAdV-scFvs, on piglet diarrhea caused by PEDV was investigated. Clinical symptoms in piglets orally challenged with PEDV, following a two-time treatment with rAdV-ZW, were significantly reduced when compared with PEDV-infected piglets treated with phosphate buffered saline (PBS) or rAdV-wild-type. Also, no death and jejunal lesions were observed. ScFv co-localization with the PEDV N protein in vivo was also observed. Next, the expression of pro-inflammatory serum cytokines such as tumor necrosis factor-α (TNF-α), IL-6, IL-8, IL-12, and IFN-λ was assessed by enzyme-linked immunosorbent assay (ELISA), which showed that scFvs significantly suppressed PEDV-induced pro-inflammatory cytokine expression and restored PEDV-inhibited IFN-λ expression. Therefore, our study supported a promising role for intracellular scFvs targeting the PEDV N protein to prevent and treat diarrhea in PEDV-infected piglets.

IntroductionSargassum fusiform is considered a traditional Chinese medicinal herb to treat many diseases, Sargassum fusiform polysaccharides (SFPS) were found to display many important biological activities. The purpose of this study was to investigate the in vitro antioxidant activity of crude polysaccharide from Sargassum fusiforme and its protective effect against H2O2-induced injury in LO2 cells.MethodsSFPS was extracted from Sargassum fusiforme using water extraction and alcohol precipitation. High-performance liquid chromatography (HPLC) was used to measure its monosaccharide composition. The in vitro antioxidant activity of SFPS was evaluated using scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl radical assays. Moreover, its hepatoprotective activity was examined by establishing H2O2-induced LO2 cells injury model.Results and discussionThe results showed that the SFPS was composed of Glc, Ara, Fuc, Gal, Man, Rha and Xyl. Meanwhile, SFPS exhibited strong antioxidant activity and potential hepatoprotective effect. Further studies found that SFPS could alleviate LO2 cells injury induced by H2O2 via decreasing malondialdehyde (MDA) and lactate dehydrogenase (LDH) levels, increasing superoxide dismutase (SOD) and catalase (CAT) activities and inhibiting intracellular reactive oxygen species (ROS) production. These results revealed that SFPS had the ability to protect the liver cells from H2O2-induced liver injury through its antioxidant activity.

Rhodobacter probiotics are considered as good alternatives to antibiotics for aquaculture. Yet the beneficial effects of Rhodobacter on Chinese mitten crab Eriocheir sinensis are still unclear, and more functions of Rhodobacter supplementation need to be clarified. In this study, a 60-day feeding trial was performed to investigate the protective effects of R. azotoformans against citrobacteriosis in E. sinensis by growth performance, serum immunity, hepatopancreatic antioxidant capability, intestinal flora, and resistance to Citrobacter freundii challenge assays. The results showed that R. azotoformans supplementation significantly and dose-dependently increased weight gain and specific growth rate as well as activities of serum immune and hepatopancreatic antioxidant enzymes, leading to notable improvement in the growth performance, serum immunity and hepatopancreatic antioxidant status of E. sinensis. Besides, R. azotoformans supplementation significantly enhanced intestinal microbial abundance and diversity in E. sinensis , and conferred significant protection of the crabs against C. freundii challenge with seven-day survival rates of 70.0%–100.0%. To the best of our knowledge, this is the first study to reveal the protective effects of R. azotoformans against citrobacteriosis in E. sinensis. Dietary supplementation with R. azotoformans significantly enhanced the protection of E. sinensis against C. freundii. [Display omitted] • R. azotoformans supplementation could improve growth performance, non-specific immunity and antioxidant capability of E. sinensis. • R. azotoformans supplementation could increase composition and diversity of the intestinal flora in E. sinensis. • R. azotoformans supplementation could confer protection of Chinese mitten crab against citrobacteriosis. [ABSTRACT FROM AUTHOR]

Human respiratory syncytial virus (HRSV) is a leading cause of lower respiratory tract infections in elderly individuals and young children/infants and can cause bronchiolitis and even death. There is no licensed HRSV vaccine. An ideal vaccine should induce high titers of neutralizing antibodies and a Th1-biased immune response. In this study, we used EXPI293 cells to express the fusion (F) protein with a prefusion conformation (PrF) and compared the safety and efficacy of intranasal immunization with PrF in combination with two mucosal adjuvants (CpG ODN and liposomes) in mice. After two intranasal administrations, mice in the PrF + CpG group produced high titers of neutralizing antibodies (4961) and a Th1-biased immune response compared with the PrF + Lipo group. The lung viral load of mice in the PrF + CpG group was significantly reduced (3.5 log) compared with that in the adjuvant control group, and the survival rate was 100 %, while the survival rate of mice in the PrF + Lipo group was only 67 %. At the same time, this immunization strategy reduced the pathological damage to the lungs in mice. In conclusion, the combination of PrF and CpG adjuvant is immunogenic, elicits a Th1 type immune response, and completely protects mice from a lethal HRSV challenge. It is worthy of further evaluation as an HRSV vaccine in clinical trials. Clinical trial registration. This study was not related to human participation or experimentation. [ABSTRACT FROM AUTHOR]

Research evidence shows that effective nutritional intervention could prevent or reduce intestinal inflammatory injury in newborn infants. Iron free lactoferrin (apo-LF), one of the main types of lactoferrin (LF), is a bioactive protein in milk that plays a vital role in maintaining intestinal health. The potential mechanism by which apo-LF modulates intestinal inflammation is, however, still unclear. In the study we first explored key genes and pathways in vitro by transcriptome date analysis and then validated them in vivo to reveal the underlying molecular mechanism. The results showed that apo-LF pretreatment effectively inhibited lipopolysaccharide (LPS)-induced primary intestinal epithelial cells (IECs) inflammation in the co-culture system (primary IECs and immune cells), which was specifically manifested as the reduction of the concentration of TNF-α, IL-6 and IL-1β and increased the concentration of IFN-γ. In addition, transcriptome data analysis revealed that the key pathway for apo-LF to exert anti-inflammatory effects was the NF-κB/PPAR signaling pathway. Further validation was performed using western blotting in colonic tissues of young mice and it was found that the major proteins of NF-κB signaling pathway (NF-κB, TNF-α and IL-1β) were inhibited by apo-LF and the target proteins of PPAR signaling pathway (PPAR-γ and PFKFB3) were activated by apo-LF. Taken together, this suggests that apo-LF has a protective effect against LPS-induced intestinal inflammatory injury via modulating the NF-κB/PPAR signaling pathway, which provides new insights for further anti-inflammatory study of apo-LF. [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.)

Abstract Background Quantitative point-of-care testing assay for detecting antibodies is critical to COVID-19 control. In this study, we established an up-conversion phosphor technology-based point-of-care testing (UPT-POCT), a lateral flow assay, for rapid COVID-19 diagnosis, as well as prediction of seral neutralizing antibody (NAb) activity and protective effects. Methods UPT-POCT was developed targeting total antibodies against the receptor-binding domain (RBD) of SARS-CoV-2 spike protein. Using ELISA as a contrast method, we evaluated the quantitation accuracy with NAb and serum samples. Cutoff for serum samples was determined through 70 healthy and 140 COVID-19 patients. We evaluated the cross-reactions with antibodies against other viruses. Then, we performed multi-center clinical trials of UPT-POCT, including 782 patients with 387 clinically confirmed COVID-19 cases. Furthermore, RBD-specific antibody levels were detected using UPT-POCT and microneutralization assay for samples from both patients and vaccinees. Specifically, the antibodies of recovered patients with recurrent positive (RP) reverse transcriptase-polymerase chain reaction test results were discussed. Results The ratios of signal intensities between the test and control bands on the lateral flow strip, namely, T/C ratios, was defined as the results of UPT-POCT. T/C ratios had excellent correlations with concentrations of NAb, as well as OD values of ELISA for serum samples. The sensitivity and specificity of UPT-POCT were 89.15% and 99.75% for 782 cases in seven hospitals in China, respectively. We evaluated RBD-specific antibodies for 528 seral samples from 213 recovered and 99 RP COVID-19 patients, along with 35 seral samples from inactivated SARS-CoV-2 vaccinees, and we discovered that the total RBD-specific antibody level indicated by T/C ratios of UPT-POCT was significantly related to the NAb titers in both COVID-19 patients (r = 0.9404, n = 527; ρ = 0.6836, n = 528) and the vaccinees (r = 0.9063, ρ = 0.7642, n = 35), and it was highly relevant to the protection rate against RP (r = 0.9886, n = 312). Conclusion This study reveals that the UPT-POCT for quantitative detection of total RBD-specific antibody could be employed as a surrogate method for rapid COVID-19 diagnosis and prediction of protective effects.

The contribution of commensal microbes to human health and disease is unknown. Bacteroides fragilis (B. fragilis) is an opportunistic pathogen and a common colonizer of the human gut. Nontoxigenic B. fragilis (NTBF) and enterotoxigenic B. fragilis (ETBF) are two kinds of B. fragilis. NTBF has been shown to affect the host immune system and interact with gut microbes and pathogenic microbes. Previous studies indicated that certain strains of B. fragilis have the potential to serve as probiotics, based on their observed relationship with the immune system. However, several recent studies have shown detrimental effects on the host when beneficial gut bacteria are found in the digestive system or elsewhere. In some pathological conditions, NTBF may have adverse reactions. This paper presents a comprehensive analysis of NTBF ecology from the host-microbe perspective, encompassing molecular disease mechanisms analysis, bacteria-bacteria interaction, bacteria-host interaction, and the intricate ecological context of the gut. Our review provides much-needed insights into the precise application of NTBF. [ABSTRACT FROM AUTHOR]

Zika virus (ZIKV) infection during pregnancy can result in severe birth defects, such as microcephaly, as well as a range of other related health complications. Heparin, a clinical-grade anticoagulant, is shown to protect neural progenitor cells from death following ZIKV infection. Although heparin can be safely used during pregnancy, it retains off-target anticoagulant effects if directly employed against ZIKV infection. In this study, we investigated the effects of chemically modified heparin derivatives with reduced anticoagulant activities. These derivatives were used as experimental probes to explore the structure–activity relationships. Precursor fractions of porcine heparin, obtained during the manufacture of conventional pharmaceutical heparin with decreased anticoagulant activities, were also explored. Interestingly, these modified heparin derivatives and precursor fractions not only prevented cell death but also inhibited the ZIKV replication of infected neural progenitor cells grown as neurospheres. These effects were observed regardless of the specific sulfation position or overall charge. Furthermore, the combination of heparin with Sofosbuvir, an antiviral licensed for the treatment of hepatitis C (HCV) that also belongs to the same Flaviviridae family as ZIKV, showed a synergistic effect. This suggested that a combination therapy approach involving heparin precursors and Sofosbuvir could be a potential strategy for the prevention or treatment of ZIKV infections.

Disturbances in the gut microbiota and its derived metabolites are closely related to the occurrence and development of hepatic steatosis. The white kidney bean (WKB), as an excellent source of protein, dietary fiber, and phytochemicals, has recently received widespread attention and might exhibit beneficial effects on a high-fat diet (HFD)-induced hepatic steatosis via targeting gut microbiota and its metabolites. The results indicated that HFD, when supplemented with WKB for 12 weeks, could potently reduce obesity symptoms, serum lipid profiles, and glucose, as well as improve the insulin resistance and liver function markers in mice, thereby alleviating hepatic steatosis. An integrated fecal microbiome and metabolomics analysis further demonstrated that WKB was able to normalize HFD-induced gut dysbiosis in mice, thereby mediating the alterations of a wide range of metabolites. Particularly, WKB remarkably increased the relative abundance of probiotics (Akkermansiaceae, Bifidobacteriaceae, and norank_f_Muribaculaceae) and inhibited the growth of hazardous bacteria (Mucispirillum, Enterorhabdus, and Dubosiella) in diet-induced hepatic steatosis mice. Moreover, the significant differential metabolites altered by WKB were annotated in lipid metabolism, which could ameliorate hepatic steatosis via regulating glycerophospholipid metabolism. This study elucidated the role of WKB from the perspective of microbiome and metabolomics in preventing nonalcoholic fatty liver disease, which provides new insights for its application in functional foods.