Hypolipidemic effect of N-acetylcysteine against dexamethasone-induced hyperlipidemia in rats

Abstract

Objective:The liver is a key metabolic organ involved in lipid metabolism and maintenance of cholesterol homeostasis in the body. However, hypercholesterolemia and oxidative stress is associated with the fatty liver which is the major risk factor associated with cardiovascular diseases (CVDs). The objective of this study was to investigate the hypolipidemic property of N-acetylcysteine (NAC) in dexamethasone-induced hyperlipidemic rats.Materials and Methods:Dexamethasone (10 mg/kg) was administered on alternate days intraperitoneally for 28 days to induce hyperlipidemia. NAC (50 mg/kg and 100 mg/kg) was daily administered intraperitoneally for 28 days. After 24 h of the last treatment blood and liver samples were collected.Results:The relative body and liver weights, activities of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lipid profile, and antioxidant defense markers were measured. The result indicated that the treatment of hyperlipidemic rats with 50 and 100 mg/kg NAC significantly (P< 0.05) prevented dexamethasone-induced body weight loss and restored liver weight. In addition, NAC reduced the elevation of hepatic enzymes activities induced by dexamethasone. Moreover, NAC exhibits hypolipidemic effect as demonstrated by reversal of serum levels of total cholesterol, triacylglycerol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and atherogenic index.Conclusion:These findings indicated that NAC was able to restore dyslipidemia induced by dexamethasone through improving liver function parameters and augments antioxidant defense systems. Altogether the anti- hyperlipidemic effects exhibited by NAC might have been mediated partly through antioxidant actions and could be beneficial against CVDs.