Abstract

To study the therapeutic effect of corn silk polysaccharide (CSP) on NAFLD mice induced by high fat diet. C57BL/6J mice were divided into normal control group (NC), high fat diet (HFD) group, HFD+200 mg/kg CSP group, and HFD+600 mg/kg CSP group. NAFLD mouse model was established by HFD feeding. Blood and liver tissues of each group were collected and biochemical and pathological tests were performed. The energy intake of NAFLD model group was higher than that of normal control group, and the food intake, water intake, and excretion of NAFLD model group were lower than that of normal control group. There was no statistical significance in the food intake, energy intake, water intake, and excretion of CSP group compared with that of NAFLD model group, nor was there any statistical significance between CSP and two doses of CSP. Biochemical tests showed that CSP decreased the levels of alanine aminotransferase, aspartate aminotransferase, triglyceride and total cholesterol in serum of HFDfed mice, and inhibited the expressions of IL-6 and TNF-α in liver tissue. Pathological results showed that CSP improved HFD-induced hepatic steatosis.

Highlights

  • Fatty liver is divided into alcoholic fatty liver disease and nonalcoholic fatty liver disease (NAFLD)[1]

  • The results showed that the liver tissue of the high fat diet (HFD) group showed a large number of vacuol-like changes of liver cells accompanied by infiltration of inflammatory cells, while hepatological changes induced by HFD were significantly reduced in the corn silk polysaccharide (CSP) treatment group

  • 3.4 CSP decreased hepatic lipid accumulation induced by HFD The results showed that the contents of TG and total cholesterol (TC) in serum of HFD group were significantly increased (P

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Summary

Introduction

Fatty liver is divided into alcoholic fatty liver disease and nonalcoholic fatty liver disease (NAFLD)[1]. NAFLD is closely related to metabolic diseases such as obesity, insulin resistance, hypertension and dyslipidemia, so NAFLD belongs to chronic metabolic abnormal liver disease[2]. Hepatocellular steatosis caused by metabolic disorders of the body at the beginning (exclusion of clear hepatic damage factors) developed into non-alcoholic steatohepatitis, followed by liver fibrosis and cirrhosis, and even eventually may lead to hepatocellular carcinoma. NAFLD is a potential factor for the development of primary hepatocellular carcinoma[3]. NAFLD affects the physical health of about 30% of adults worldwide[4]. NAFLD has become a public health problem closely related to our life. Many strategies have been developed for the treatment of NAFLD, there are currently no drugs specific for NAFLD

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