Article,

Quercetin through mitigation of inflammatory response and oxidative stress exerts protective effects in rat model of diclofenac-induced liver toxicity

, , , , and .
Journal of Pharmacy & Pharmacognosy Research, 7 (3): 200-212 (May 2019)

Abstract

Context: Diclofenac (DIC) is known for its anti-inflammatory and analgesic properties but liver toxicity is one of the main targets to use this drug. Previous studies have demonstrated that quercetin may decrease the toxicity of synthetic drugs. Aim: To assess the protective effect of quercetin against DIC-induced liver toxicity in rats. Methods: The rats exposed to DIC (50 mg/kg; i.p.) were treated with different doses of quercetin (20, 40 and 80 mg/kg). The levels of glutathione peroxidase (GPx), superoxide dismutase (SOD), intracellular glutathione (GSH) and catalase (CAT) in the liver tissue were assessed. Results: Results indicated a significant decline in above-mentioned factors in DIC-alone treated group compared to the control group. Also, levels of the triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), total bilirubin, alkaline phosphatase (ALP), nitrite content, alanine aminotransferase (ALT), malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α), serum interleukin-1β (IL-1β), aspartate aminotransferase (AST), and inflammatory cytokines were evaluated and results indicted remarkable elevation in these factors in DIC-alone treated group compared to the control group. Treatment with quercetin caused a significant elevation in GPx, SOD, GSH, CAT and a significant reduction in levels of TG, TC, LDL-C, VLDL-C, total bilirubin, ALP, nitrite content, ALT, MDA, serum TNF-α, serum IL-1β, AST and inflammatory cytokines in DIC-alone treated group compared to the control group (p<0.05). Histopathological alterations were also improved following quercetin administration. Conclusions: Quercetin may exert a protective effect against DIC-induced liver toxicity in rats through mitigation of oxidative stress and inflammatory response.

Tags

Users

  • @jppres

Comments and Reviews