Bergenin Attenuates Hepatic Fibrosis by Regulating Autophagy Mediated by the PPAR-γ/TGF-β Pathway.

Yujing Xia,Jingjing Li,Chuanyong Guo,Jiao Feng,Kan Chen,Ravinder K Kaundal

doi:10.1155/2020/6694214

Abstract

Liver fibrosis is a pathological process involving diffuse extracellular matrix (ECM) deposition in the liver. It is typical of many chronic liver diseases, including cirrhosis, and effective drugs are needed. In this study, we explored the protective effect of bergenin on liver fibrosis induced by carbon tetrachloride and bile duct ligation. A variety of molecular biological methods (qRT-PCR, western blotting, and immunohistochemistry) were employed to confirm the increased degree of hepatocyte injury and ECM formation in the disease model, consistent with autophagy and activation of the TGF-β pathway. Bergenin activated PPAR-γ and inhibited TGF-β and autophagy and decreased liver fibrosis by inhibiting hepatocyte necrosis and ECM formation in a dose-dependent manner. The results suggest that bergenin may be a promising drug candidate for the treatment of liver fibrosis.

Highlights

Liver fibrosis is a pathophysiological process in which various pathogenic factors continually damage the liver, resulting in extracellular matrix (ECM) deposition and fibrous scar formation [1]
Liver enzymes and hydroxyproline are important indicators that reflect the severity of liver fibrosis; serum and pathological examination was carried out to evaluate the effects of the drug
The results showed that levels of ALT and AST in the CCl4 and BDL groups were increased, while levels of liver enzymes in drug treatment groups were significantly decreased, and the effect was more obvious with an increasing dose (Figure 1(a))

Summary

Introduction

Liver fibrosis is a pathophysiological process in which various pathogenic factors continually damage the liver, resulting in extracellular matrix (ECM) deposition and fibrous scar formation [1]. More than one million people worldwide die of end-stage liver disease caused by liver fibrosis every year [2]. In recent years, experts in the field have explored treatments for liver diseases, especially liver fibrosis and cirrhosis. PPAR-γ is a key transcription factor of cell differentiation, which is closely related to fibrosis in important organs [5, 6]. PPAR-γ is involved in hepatic stellate cell (HSC) activation and fibroblast transformation, which can reduce the overexpression of α-smooth muscle actin

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