disorders. However, Px is known to induce gastric ulceration and hepato-renal toxicity. Rosuvastatin (ROSV), a
member of the statin family, has anti-inflammatory and antioxidant actions independent of its anti-hyperlipidemic
action. Therefore, we investigated the protective effects of ROSV against Px-induced gastric, liver, and
kidney injury. Five groups of seven rats each were used; control group, ROSV group (20 mg/kg, given orally), Px
group (7 mg/kg, given intraperitoneally), Px+ROSV L (7 and 10 mg/kg, respectively), and Px+ROSV H (7 and
20 mg/kg, respectively) group. The results revealed that Px induced severe gastric mucosal damage expressed by
high ulcer index along with significant increases in liver and kidney function parameters including AST, ALT,
creatinine, and urea. Disrupted lipid metabolism also was observed in Px-treated animals. Moreover, marked an
increase in malondialdehyde (MDA) and decreases in glutathione (GSH) and catalase (CAT) levels along with
enhanced activated caspase-3 expression in the gastric, hepatic, and renal tissues following Px-insult suggested a
possible involvement of lipid peroxidation in Px-induced gastropathy and hepatorenal toxicity. However, in a
dose-dependent manner, ROSV was able to mitigate Px-induced lipid peroxidation and apoptosis in gastric, liver,
and kidney tissues.