Prevention of Nonalcoholic Hepatic Steatosis by Shenling Baizhu Powder: Involvement of Adiponectin-Induced Inhibition of Hepatic SREBP-1c.

Kairui Tang,Jiqian Xie,Qinhe Yang,Yupei Zhang,Chuiyang Zheng,Huan Nie,Yuanjun Deng,Runsen Chen,Maoxing Pan

doi:10.1155/2020/9701285

Abstract

Background Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its incidence is increasing annually, but there is currently no specific drug for treating NAFLD. Shenling Baizhu powder (SL) is a safe herbal compound commonly used in clinical practice. Our previous research has shown that SL has the effect of preventing NAFLD, but its specific mechanism has not been determined. In this study, the potential mechanism of SL on NAFLD was explored by in vivo experiments. Methods Wistar rats fed a choline-deficient amino acid-defined diet (CDAA) were treated with SL for 8 weeks. Then, serum samples were collected to obtain biochemical indicators; adipose tissue and liver samples were collected for pathological detection; a moorFLPI-2 blood flow imager was used to measure liver microcirculation blood flow, and a rat cytokine array was used to screen potential target proteins. The expression of liver adiponectin/SREBP-1c pathway-related proteins was determined by Western blotting. Results SL effectively reduced the liver wet weight, as well as the levels of total cholesterol (TC) and triglyceride (TG) in the liver, and ameliorated liver injury in CDAA-fed rats. Pathological examinations showed that SL markedly reduced liver lipid droplets and improved liver lipid accumulation. In addition, the detection of liver blood flow showed that SL increased liver microcirculation in CDAA-fed rats. Through the cytokine array, a differentially expressed cytokine, namely, adiponectin, was screened in the liver. Western blotting assays showed that SL increased the expression of adiponectin and phosphoacetyl-CoA Carboxylase (p-ACC) in the liver and decreased the expression of steroid regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS). Conclusion These results suggest that SL can increase the levels of adiponectin in the liver and serum and can inhibit the expression of SREBP-1c, thereby regulating systemic lipid metabolism and reducing liver lipid accumulation.

Highlights

Nonalcoholic fatty liver disease is a clinicopathological syndrome characterized by excessive lipid deposition in hepatocytes in the absence of alcohol and other causes of liver damage
The body weight of each group increased gradually, and there was no significant difference in body weight between the choline-sufficient amino acid-defined diet (CSAA) group and the choline-deficient amino acid-defined diet (CDAA) group
When measuring visceral white fat, it was found that the weight of perirenal fat pads of rats fed with CDAA diet was significantly lower than that of CSAA group (P < 0:05), while the epididymal fat pads of the CDAA group showed a tendency to decrease, suggesting that the choline deficiency diet-induced Nonalcoholic fatty liver disease (NAFLD) rat model in this study may be related to these changes in visceral fat [20]

Summary

Introduction

Nonalcoholic fatty liver disease is a clinicopathological syndrome characterized by excessive lipid deposition in hepatocytes in the absence of alcohol and other causes of liver damage. Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its incidence is increasing annually, but there is currently no specific drug for treating NAFLD. Serum samples were collected to obtain biochemical indicators; adipose tissue and liver samples were collected for pathological detection; a moorFLPI-2 blood flow imager was used to measure liver microcirculation blood flow, and a rat cytokine array was used to screen potential target proteins. Western blotting assays showed that SL increased the expression of adiponectin and phosphoacetyl-CoA Carboxylase (p-ACC) in the liver and decreased the expression of steroid regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS). These results suggest that SL can increase the levels of adiponectin in the liver and serum and can inhibit the expression of SREBP-1c, thereby regulating systemic lipid metabolism and reducing liver lipid accumulation

Methods

Results

Conclusion