Abstract

This study evaluated the protective effects of aqueous extract of Lycium barbarum (LBAE) and ethanol extract of Lycium barbarum (LBEE) on blood lipid levels, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activities and liver tissue antioxidant enzyme activities in rats fed a high fat diet (HF). The rats were randomly divided into seven groups of ten rats each and fed a different diet for eight weeks as follows: One group (NC group) was fed a standard diet, one group was fed a high-fat diet (HF group), one group was fed a high-fat diet and orally fed with 20 mg/kg b.w. simvastatin (HF + simvastatin group), and the other group was fed the high fat diet and orally fed with 50 mg/kg b.w. or 100 mg/kg b.w. LBAE (HF + LBAE), or 50 mg/kg b.w. or 100 mg/kg b.w. LBEE (HF + LBEE), respectively. After eight weeks, the HF diet caused deleterious metabolic effects. Rats fed the HF diet alone showed increased hepatocellular enzyme activities in plasma, a significant decline in antioxidant enzyme activities, and elevated liver lipid peroxidation indices. LBAE and LBEE administration significantly reduced liver damage and oxidative changes, and brought back the antioxidants and lipids towards normal levels. These data suggest that these antioxidants protect against toxicity parameters in HF rats.

Highlights

  • Reactive oxygen species (ROS) have detrimental effects on hepatocytes by damaging DNA, lipids, and proteins, leading to disruption in cellular homeostasis and aggravating metabolic syndrome features [1]

  • In some people with Nonalcoholic fatty liver disease (NAFLD), the excess fat in the liver causes necroinflammatory changes to the liver cell, which can progress to fibrosis and cirrhosis, and potentially, HCC

  • The current study examined the effects of Lycium barbarum aqueous and ethanol extracts on oxidative stress and antioxidant enzymes in the liver of rats fed a high-fat diet

Read more

Summary

Introduction

Reactive oxygen species (ROS) have detrimental effects on hepatocytes by damaging DNA, lipids, and proteins, leading to disruption in cellular homeostasis and aggravating metabolic syndrome features [1]. ROS damage cellular macromolecules causing lipid peroxidation and nucleic acid and protein alterations. Their formation is considered as a pathobiochemical mechanism involved in the initiation or progression phases of various diseases such as atherosclerosis, ischemic heart diseases, diabetes, initiation of carcinogenesis or liver diseases [2,3,4,5]. NAFLD is found in at least 20% of the population in developed countries and is linked with obestiy, insulin resistance and the metabolic syndrome. In some people with NAFLD, the excess fat in the liver (steatosis) causes necroinflammatory changes to the liver cell (nonalcoholic steatohepatisis [NASH]), which can progress to fibrosis and cirrhosis, and potentially, HCC. NASH affects 2–3% of the adult population in western country

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call