Abstract
Huo-Xue-Qu-Yu formula (HXQYF) is a prescription consisting of Ginkgo biloba leaf and Paeonia lactiflora Pall. for treating hyperlipidemia and NAFLD in China. Here, we investigated the hepatic and renal function, oxidative stress and lipid metabolism, and potential mechanisms of HXQYF on nonalcoholic fatty liver disease (NAFLD) rat models. NAFLD rat models were induced with high-fat diet (HFD) and 10% fructose water for 18 weeks and orally administered with or without HXQYF simultaneously. The results showed that HXQYF (22.5, 45, 90 mg/kg) significantly improved blood lipid levels via reducing serum TC, TG, LDL-C, and APOB values and elevating HDL-C and APOA1 levels in NAFLD rats. The higher levels of ALT, AST, CR, and BUN in serum induced by HFD were reduced by HXQYF. HE staining showed that HXQYF (90 mg/kg) reduced the accumulation of fat droplets and alleviated inflammatory response in liver cells. Three doses of HXQYF exhibited notable antioxidant effects by elevating SOD, GSH, and CAT activities and decreasing MDA and OH-1 levels in the liver. Furthermore, abnormal lipid metabolism caused by HFD was alleviated by HXQYF, which was associated with the upregulation of PPAR-α, AdipoR2, and CPT1 mRNAs as well as the downregulation of CYP2E1 and SREBP-1c mRNAs in liver tissue. In conclusion, our work verified that HXQYF could reduce the degree of hepatic steatosis, suppress oxidative stress, and attenuate lipid metabolism, thus preventing NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD), a most common chronic liver disease, arises from the modern lifestyle, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and eventually to hepatocellular carcinoma (HCC) [1]. e increasing prevalence of NAFLD is associated with obesity, hypertension, and dyslipidemia, and diabetes [2, 3]
Excessive lipid accumulation in the liver plays an essential role in developing NAFLD; and the production of reactive oxygen species (ROS) is enhanced in both patients with and animal models of NAFLD [8, 9]. erefore, it will be of interest to target on regulating lipid metabolism, oxidative stress, and inflammatory response for the prevention of the progression of NAFLD
The results showed that expressions of Adiponectin receptor 2 (AdipoR2), PPAR-α, and CPT1 mRNAs in the liver of NAFLD rats were significantly downregulated, which were reversed by treatment with Huo-Xue-Qu-Yu formula (HXQYF) (45 mg/kg) in NAFLD rats
Summary
Nonalcoholic fatty liver disease (NAFLD), a most common chronic liver disease, arises from the modern lifestyle, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and eventually to hepatocellular carcinoma (HCC) [1]. e increasing prevalence of NAFLD is associated with obesity, hypertension, and dyslipidemia, and diabetes [2, 3]. E increasing prevalence of NAFLD is associated with obesity, hypertension, and dyslipidemia, and diabetes [2, 3]. It increased the risk of developing diseases such as cirrhosis, extrahepatic cancers, cardiovascular disease, type 2 diabetes mellitus (T2DM), and chronic kidney disease [4]. Genetic factors, metabolic factors, and environmental factors were cooperated to promote the accumulation of fat in hepatocytes and successively cause inflammation and fibrosis [6]. Adipose tissue and muscle could promote inflammation and oxidative stress in the liver [7]. Erefore, it will be of interest to target on regulating lipid metabolism, oxidative stress, and inflammatory response for the prevention of the progression of NAFLD Excessive lipid accumulation in the liver plays an essential role in developing NAFLD; and the production of reactive oxygen species (ROS) is enhanced in both patients with and animal models of NAFLD [8, 9]. erefore, it will be of interest to target on regulating lipid metabolism, oxidative stress, and inflammatory response for the prevention of the progression of NAFLD
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