Yu Gan Long Ameliorates Hepatic Fibrosis by Inhibiting PI3K/AKT,Ras/ERK and JAK1/STAT3 Signaling Pathways in CCl4-induced Liver Fibrosis Rats
作者机构:Hubei Key Laboratory of Resources and Chemistry of Chinese MedicineHubei University of Chinese MedicineWuhan430065China College of PharmacyHubei University of Chinese MedicineWuhan430065China Wuhan Junan Pharmaceutical Co.Ltd.Wuhan430023China
出 版 物:《Current Medical Science》 (当代医学科学(英文))
年 卷 期:2020年第40卷第3期
页 面:539-547页
核心收录:
学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金:This study was supported by grants from China Postdoctoral Science Foundation(No.2016M592320,No.2016M600670) Hubei Provincial Natural Science Foundation of China(No.2018CFB657) the National Natural Science Foundation of China(No.81601605)
主 题:Yu Gan Long traditional Chinese herbal therapy liver fibrosis Ras/ERK PI3K/AKT JAK1/STAT3
摘 要:Yu Gan Long(YGL)is a Chinese traditional herbal formula which has been reported to attenuate liver fibrosis for many years and we have explored its anti-fibrotic mechanism through blocking transforming growth factor(TGF-β)in the previous *** the mechanisms associated with platelet-derived growth factor(PDGF)-BB remain *** this study,we further investigated the mechanism of YGL reducing carbon tetrachloride(CCl4)-induced liver fibrosis in *** results showed that YGL suppressed CCl4-induced upregulation of collagen IV(Col IV),type HI precollagen(PCHI),hyaluronuc acid(HA)and laminin(LN),which are implicated in liver ***,YGL reduced theα-smooth muscle actin(α-SMA)expression,which acts as the indicator of liver ***,YGL decreased the serum levels of hepatic stellate cell(HSC)mitogen PDGF-BB and inflammation cytokines,including TNF-α,IL-1β,*** involved in liver fibrosis,such as Ras,p-Raf-1,p-ERK1/2,p-JNK,p-P38,p-PI3K,p-AKT,p-JAKl,p-STAT3 were downregulated significantly after treatment with *** results indicated that YGL ameliorated CCl4-induced liver fibrosis by reducing inflammation cytokines production,and suppressing Ras/ERK,PI3K/AKT,and JAK1/STAT3 signaling pathways,which provided further evidence towards elucidation of the anti-fibrotic mechanism of YGL.