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10.2147/DDDT.S85426 http://scihub22266oqcxt.onion/10.2147/DDDT.S85426 C4529259!4529259 !26347199     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26347199 &cmd=llinks): Failed to open stream: HTTP request failed! 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9 (ä): 3989-4104 Nephropedia Template TP {{tp|p=26347199 |t=2015. A bioinformatic and mechanistic study elicits the antifibrotic effect of ursolic acid through the attenuation of oxidative stress with the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in human hepatic stellate cells and rat liver |pdf=|usr=}}{{26347199 }} gab.com Text A bioinformatic and mechanistic study elicits the antifibrotic effect of ursolic acid through the attenuation of oxidative stress with the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in human hepatic stellate cells and rat liver JO: Drug Des Devel Ther http://www.kidney.de/pget.php?&tw=1&pmid=26347199 #FOAvip NADPH oxidases (NOXs) are a predominant mediator of redox homeostasis in hepatic stellate cells (HSCs), and oxidative stress plays an important role in the pathogenesis of liver fibrosis. Ursolic acid (UA) is a pentacyclic triterpenoid with various pharmacological activities, but the molecular targets and underlying mechanisms for its antifibrotic effect in the liver remain elusive. This study aimed to computationally predict the molecular interactome and mechanistically investigate the antifibrotic effect of UA on oxidative stress, with a focus on NOX4 activity and cross-linked signaling pathways in human HSCs and rat liver. Drug-drug interaction via chemical-protein interactome tool, a server that can predict drug-drug interaction via chemical-protein interactome, was used to predict the molecular targets of UA, and Database for Annotation, Visualization, and Integrated Discovery was employed to analyze the signaling pathways of the predicted targets of UA. The bioinformatic data showed that there were 611 molecular proteins possibly interacting with UA and that there were over 49 functional clusters responding to UA. The subsequential benchmarking data showed that UA significantly reduced the accumulation of type I collagen in HSCs in rat liver, increased the expression level of MMP-1, but decreased the expression level of TIMP-1 in HSC-T6 cells. UA also remarkably reduced the gene expression level of type I collagen in HSC-T6 cells. Furthermore, UA remarkably attenuated oxidative stress via negative regulation of NOX4 activity and expression in HSC-T6 cells. The employment of specific chemical inhibitors, SB203580, LY294002, PD98059, and AG490, demonstrated the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in the regulatory effect of UA on NOX4 activity and expression. Collectively, the antifibrotic effect of UA is partially due to the oxidative stress attenuating effect through manipulating NOX4 activity and expression. The results suggest that UA may act as a promising antifibrotic agent. More studies are warranted to evaluate the safety and efficacy of UA in the treatment of liver fibrosis. Twit Text FOAVip A bioinformatic and mechanistic study elicits the antifibrotic effect of ursolic acid through the attenuation of oxidative stress with the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in human hepatic stellate cells and rat liver ????Drug Des Devel Ther http://www.kidney.de/pget.php?&tw=1&pmid=26347199 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26347199 #FOAvip English Wikipedia <ref>{{Cite pmid|26347199 }}</ref> A bioinformatic and mechanistic study elicits the antifibrotic effect of ursolic acid through the attenuation of oxidative stress with the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in human hepatic stellate cells and rat liver #MMPMID26347199 He W ; Shi F ; Zhou ZW ; Li B ; Zhang K ; Zhang X ; Ouyang C ; Zhou SF ; Zhu X Drug Des Devel Ther 2015[]; 9 (ä): 3989-4104 PMID26347199 show ga NADPH oxidases (NOXs) are a predominant mediator of redox homeostasis in hepatic stellate cells (HSCs), and oxidative stress plays an important role in the pathogenesis of liver fibrosis. Ursolic acid (UA) is a pentacyclic triterpenoid with various pharmacological activities, but the molecular targets and underlying mechanisms for its antifibrotic effect in the liver remain elusive. This study aimed to computationally predict the molecular interactome and mechanistically investigate the antifibrotic effect of UA on oxidative stress, with a focus on NOX4 activity and cross-linked signaling pathways in human HSCs and rat liver. Drug-drug interaction via chemical-protein interactome tool, a server that can predict drug-drug interaction via chemical-protein interactome, was used to predict the molecular targets of UA, and Database for Annotation, Visualization, and Integrated Discovery was employed to analyze the signaling pathways of the predicted targets of UA. The bioinformatic data showed that there were 611 molecular proteins possibly interacting with UA and that there were over 49 functional clusters responding to UA. The subsequential benchmarking data showed that UA significantly reduced the accumulation of type I collagen in HSCs in rat liver, increased the expression level of MMP-1, but decreased the expression level of TIMP-1 in HSC-T6 cells. UA also remarkably reduced the gene expression level of type I collagen in HSC-T6 cells. Furthermore, UA remarkably attenuated oxidative stress via negative regulation of NOX4 activity and expression in HSC-T6 cells. The employment of specific chemical inhibitors, SB203580, LY294002, PD98059, and AG490, demonstrated the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in the regulatory effect of UA on NOX4 activity and expression. Collectively, the antifibrotic effect of UA is partially due to the oxidative stress attenuating effect through manipulating NOX4 activity and expression. The results suggest that UA may act as a promising antifibrotic agent. More studies are warranted to evaluate the safety and efficacy of UA in the treatment of liver fibrosis. |*Computational Biology [MESH] |Animals [MESH] |Antioxidants/*pharmacology [MESH] |Cell Line [MESH] |Cell Proliferation/drug effects [MESH] |Collagen Type I/genetics/metabolism [MESH] |Dimethylnitrosamine [MESH] |Dose-Response Relationship, Drug [MESH] |Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/*metabolism [MESH] |Gene Expression Regulation [MESH] |Hepatic Stellate Cells/*drug effects/enzymology/pathology [MESH] |Humans [MESH] |Liver Cirrhosis, Experimental/chemically induced/*drug therapy/enzymology/pathology [MESH] |Liver/*drug effects/enzymology/pathology [MESH] |Male [MESH] |Matrix Metalloproteinase 1/metabolism [MESH] |NADPH Oxidase 4 [MESH] |NADPH Oxidases/metabolism [MESH] |Oxidative Stress/*drug effects [MESH] |Phosphatidylinositol 3-Kinase/*metabolism [MESH] |Phosphoinositide-3 Kinase Inhibitors [MESH] |Protein Interaction Maps [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism [MESH] |Rats, Sprague-Dawley [MESH] |Signal Transduction/drug effects [MESH] |Time Factors [MESH] |Tissue Inhibitor of Metalloproteinase-1/metabolism [MESH] |Triterpenes/*pharmacology [MESH] |Ursolic Acid [MESH]A bioinformatic and mechanistic study elicits the antifibrotic effect (epmc).pdf DeepDyve Pubget Overpricing