Hepatoprotective activity of quercetin against paracetamol-induced liver toxicity in rats

Abstract

Background Paracetamol (PCM) overdose induces hepatotoxicity in both humans and experimental animals. The pathogenesis and progression of PCM hepatic toxicity are associated with free radical injury and oxidative stress, which could be partially attenuated by antioxidants and free radical scavengers. Aim The present study was undertaken to examine the effects of quercetin on PCM-induced hepatic toxicity in rats. Material and methods In this experimental study, forty adult male rats were divided into four groups: control, quercetin, PCM groups, and the protective group that was pretreated with quercetin orally [50 mg/kg body weight (b.w.)] daily for 16 days and thereafter received both quercetin (same dose) and PCM (500 mg/kg b.w.) for another 5 days. Twenty-four hours after the administration of PCM, the rats were killed to measure serum hepatotoxic markers, levels of tumor necrosis factor-α, and oxidative stress biomarkers. Results Oral administration of PCM (500 mg/kg b.w.) for 5 days resulted in a significant elevation of liver enzymes in serum such as aspartate transaminase, alanine transaminase, alkaline phosphatase, and total bilirubin, and in levels of tumor necrosis factor-α as well as reducing hepatic total protein and albumin concentrations when compared with the results in the control group. As regards oxidative stress biomarkers, there were increased tissue levels of malondialdehyde and decreases in the activity of liver enzymes [superoxide dismutase, catalase, glutathione, glutathione peroxidase, and glutathione-s-transferase] in the group treated with PCM. All of these results were ameliorated by coadministration of quercetin. Conclusion These results suggest that the protective role of quercetin in the prevention of PCM-induced hepatic toxicity in rats was associated with a decrease of oxidative stress in hepatic tissues. However, clinical studies are warranted to investigate such an effect in humans.