Abstract

Qushi Huayu Decoction (QHD), a Chinese herbal formula, has been proven effective on alleviating nonalcoholic fatty liver disease (NAFLD) in human and rats. The present study was conducted to investigate whether QHD could inhibit hepatic lipid accumulation by activating AMP-activated protein kinase (AMPK) in vivo and in vitro. Nonalcoholic fatty liver (NAFL) model was duplicated with high-fat diet in rats and with free fatty acid (FFA) in L02 cells. In in vivo experimental condition, QHD significantly decreased the accumulation of fatty droplets in livers, lowered low-density lipoprotein cholesterol (LDL-c), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels in serum. Moreover, QHD supplementation reversed the HFD-induced decrease in the phosphorylation levels of AMPK and acetyl-CoA carboxylase (ACC) and decreased hepatic nuclear protein expression of sterol regulatory element-binding protein-1 (SREBP-1) and carbohydrate-responsive element-binding protein (ChREBP) in the liver. In in vitro, QHD-containing serum decreased the cellular TG content and alleviated the accumulation of fatty droplets in L02 cells. QHD supplementation reversed the FFA-induced decrease in the phosphorylation levels of AMPK and ACC and decreased the hepatic nuclear protein expression of SREBP-1 and ChREBP. Overall results suggest that QHD has significant effect on inhibiting hepatic lipid accumulation via AMPK pathway in vivo and in vitro.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is an increasingly common health concern that it is considered to be a component of the metabolic syndrome

  • The spectrum of NAFLD can range from simple fatty liver, with a begin prognosis, to the potentially progressive form of nonalcoholic steatohepatitis (NASH), which can lead to fibrosis and cirrhosis [1, 2]

  • The High-Pressure Liquid Chromatography (HPLC) chromatogram showed that chlorogenic acid, polygonin, resveratrol, and jasminoidin in Qushi Huayu Decoction (QHD) were well resolved by gradient elution (Figure 1)

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is an increasingly common health concern that it is considered to be a component of the metabolic syndrome. The spectrum of NAFLD can range from simple fatty liver (hepatic steatosis), with a begin prognosis, to the potentially progressive form of nonalcoholic steatohepatitis (NASH), which can lead to fibrosis and cirrhosis [1, 2]. The origin of this disease is unknown and probably multifactorial [3]. Considering the key role of AMPK activation in the regulation of lipid metabolism and the potential capability of QHD in preventing hepatic steatosis, we hypothesized that AMPK might be a mediator due to the effects of QHD. We observed the effect of QHD on AMPK activation and the related pathways in hepatic lipogenesis in high-fat diet-induced obese rats and in FFA-induced steatosis L02 cells

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