Curcumin Alleviates Potassium Bromate-Induced Hepatic Damage by Repressing CRP Induction through TNF-α and IL-1β and by Suppressing Oxidative Stress

Abstract

This study evaluated the prospective molecular and biochemical mechanisms behind the hepatoprotective effects of curcumin in Wistar rats exposed to KBrO3. Techniques for assessment of hepatic oxidative injury and histological biomarkers were used. The concentrations of proteins connected with inflammation (e.g. tumor necrosis factor-alpha (TNF-α), interleukins 1β (IL-1β) and C-reactive protein (CRP)) were estimated by enzyme-linked immunosorbent assay (ELISA) techniques. Results showed that, curcumin administered orally at a dose of 20 mg/kg for 28 days significantly suppressed the activities of serum transaminases and alkaline induced by KBrO3 administration (20 mg/kg, twice weekly) and protected the integrity of the liver tissue. Also, curcumin at the tested dose abridged the KBrO3-induced increase in hepatic malondialdehyde (MDA) levels and reversed KBrO3 mediated reduction in activities of hepatic antioxidant molecules including reduced glutathione (GSH), total thiol (TSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD). In addition, curcumin significantly assuaged inflammatory response in KBrO3-lesioned liver as revealed by the decrease in inflammatory biomarkers. This study suggests that curcumin exhibits a protective effect via induction of hepatic detoxification proteins and inhibition of inflammatory proteins in addition to its antioxidative ability in KBrO3- induced hepatic injury in rats.