| 1 | Lycium barbarum polysaccharides ameliorate canine acute liver injury by reducing oxidative stress,protecting mitochondrial function,and regulating metabolic pathways显示文摘The development of acute liver injury can result in liver cirrhosis,liver failure,and even liver cancer,yet there is currently no effective therapy for it.The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lycium barbarum polysaccharides(LBPs)on acute liver injury induced by carbon tetrachloride(CCl_(4)).To create a model of acute liver injury,experimental canines received an intraperitoneal injection of 1 mL/kg of CCl_(4)solution.The experimental canines in the therapy group were then fed LBPs(20 mg/kg).CCl_(4)-induced liver structural damage,excessive fibrosis,and reduced mitochondrial density were all improved by LBPs,according to microstructure data.By suppressing Kelch-like epichlorohydrin(ECH)-associated protein 1(Keap1),promoting the production of sequestosome 1(SQSTM1)/p62,nuclear factor erythroid 2-related factor 2(Nrf2),and phaseⅡdetoxification genes and proteins downstream of Nrf2,and restoring the activity of anti-oxidant enzymes like catalase(CAT),LBPs can restore and increase the antioxidant capacity of liver.To lessen mitochondrial damage,LBPs can also enhance mitochondrial respiration,raise tissue adenosine triphosphate(ATP)levels,and reactivate the respiratory chain complexes I–V.According to serum metabolomics,the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism.9-Hydroxyoctadecadienoic acid(9-HODE),lysophosphatidylcholine(Lyso PC/LPC),and phosphatidylethanolamine(PE)may be potential indicators of acute liver injury.This study confirmed that LBPs,an effective hepatoprotective drug,may cure acute liver injury by lowering oxidative stress,repairing mitochondrial damage,and regulating metabolic pathways. | JIANJIA HUANG YUMAN BAI WENTING XIE RONGMEI WANG WENYUE QIU SHUILIAN ZHOU ZHAOXIN TANG JIANZHAO LIAO RONGSHENG SU | 2023 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2023，24，2： | 2 |
| 7 | Based on network pharmacology to explore the mechanism of nephrotoxicity of Xanthii Fructus显示文摘Objective:To explore the potential mechanism of nephrotoxicity induced by Xanthii Fructus(XF)through network pharmacology.Methods:The active ingredients and targets of XF were screened through Traditional Chinese Medicine Systems Pharmacology Database,PubChem Database and Swiss Target Prediction Database,and the related pathogenic genes of nephrotoxicity were downloaded from Genecards,pharmGKB and OMIM databases.The potential target is the intersection of XF and the pathogenic gene of nephrotoxicity.Cytoscape software was used to construct a network of“XF-Potential active ingredient-Target-Nephrotoxicity network”.Protein protein interaction(PPI)network was constructed by String database,and the data was analyzed and sorted out to obtain the key active components and core target proteins of XF.GO functional enrichment analysis and KEGG pathway enrichment analysis of key target proteins were performed by R software.Results:11 active components,167 targets,6839 nephrotoxicity related pathogenic genes and 139 intersection target genes were screened from XF.After constructing the network of“XF-Potential active ingredient-target-nephrotoxicity network”and PPI network,the key active ingredients of XF were identified as Moupinamide,Beta-sitosterol and Stigmasterol,and the core target proteins were CASP3,HSP90AA1 and TP53.There were 2072 GO entries(P<0.05),including 1876 Biological Process(BP),64 Cellular Component(CC)and 132 Molecular Function(MF).KEGG enrichment analysis revealed 138 pathways(P<0.05),mainly involving p53 signaling pathway,IL-17 signaling pathway,PI3K-Akt signaling pathway were strongly correlated with the nephrotoxicity of XF.Conclusion:The core target protein of XF HSP90AA1,CASP3 and TP53 participate in p53 signaling Pathway,PI3K-Akt signaling Pathway,IL-17 signaling Pathway and other pathways to regulate apoptosis and induce inflammatory responses,resulting in kidney damage. | Tao Chen Tengda Li Wenna Zhang Yulin Song Yuman Tang Rui Gong Hua Jin | 2022 | Asian Toxicology Tesearch2022，4，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员