Protective effect of gallic acid against thioacetamide-induced metabolic dysfunction of lipids in hepatic and renal toxicity

Abstract

BackgroundGallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. MethodsThe current study looked at the effect of gallic acid (GA) (100 mg, 200 mg/kg orally) on liver and kidney damage caused by thioacetamide (TAA; 100 mg/Kg via intraperitoneal route). TAA was treated thrice weekly for eight weeks, whereas gallic acid was administered daily. ResultsGA alleviated the thioacetamide-induced decreases in hepatic or renal reduced glutathione (GSH) or increases in malondialdehyde (MDA, an indication of lipid peroxidation). TAA treatment significantly increased plasma inflammatory markers, tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), liver enzymes, Gamma-glutamyltransferase (GGT), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), alkaline phosphatase (ALP), and kidney function parameters (creatinine and urea) and uric acid. However, these values decreased after GA treatment in a dose-dependent manner. Furthermore, GA mitigated the considerable decrease in plasma protein caused by TAA. GA also reduced hepatic fibrosis or histological abnormalities in the liver and kidney. ConclusionOur results suggest that GA may attenuate TAA-induced liver and kidney toxicity via suppression of oxidative stress and inflammatory markers. Moreover, the hypolipidemic effect of GA may be considered another route for protection.