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

Abstract

Background: Gallic acid (GA) has significant antioxidant bioactivity and can prevent diet-induced hypertriglyceridemia by reducing adipocytes. GA was also observed to enhance cell glucose uptake. Methods: The 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. Results: GA 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. Conclusion: Our 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.

Keywords

• Gallic acid
• Thioacetamide hepatic injury
• Kidney injury
• Oxidative stress
• Inflammatory markers