Suppression of Diabetes-Induced Liver Injury and Fibrosis by Resveratrol in Association with the Inhibition of the ROS/CD86/Inflammation Axis and Protection of Liver Glycogen Stores
摘要
We recently reported the expression of the immune biomarker cluster of differentiation 86 (CD86) in the hepatic tissue of diabetic rats. However, the association between oxidative stress (ROS), CD86, inflammation, and liver fibrosis induced by diabetes—with and without treatment using the pleiotropic polyphenol resveratrol—has not been previously investigated.
MethodsType 2 diabetes mellitus (T2DM) was induced in rats. The protective group started resveratrol (30 mg/kg) treatment 14 days before the induction of diabetes and continued on resveratrol until sacrifice at week 12.
ResultsDiabetes-induced liver injury was confirmed by substantial tissue damage, hepatocyte ultrastructural alterations, depletion of liver glycogen stores, and collagen deposition (fibrosis). Diabetes also significantly increased blood levels of ROS and inflammatory biomarkers, as well as hepatic tissue levels of CD86 mRNA and the biomarker of fibrosis, TIMP-1. All these diabetic complications were significantly inhibited by resveratrol.
ConclusionThis study highlights a strong association between the ROS/CD86/inflammation axis and diabetes-induced liver injury and fibrosis. Resveratrol exerted significant protective effects, suggesting its potential as a therapeutic agent for managing liver complications secondary to diabetes.