The Effects of Astaxanthin on Ischemia-Reperfusion Induced Renal Functional and Histopathological Disturbances in Rats: Relevance to Its Antioxidant Effects

Background: Ischemia-reperfusion (I/R) injury is a leading cause of acute renal failure, primarily driven by oxidative stress and inflammation, resulting in renal cell dysfunction and damage. Objectives: This study aims to evaluate the effects of astaxanthin (AST), a potent antioxidant and anti-inflammatory carotenoid, against renal I/R injury in a rat model. Methods: A total of 30 male Wistar rats were randomly assigned to five groups: A sham group, an I/R group, and three groups treated with AST at doses of 5, 10, and 15 mg/kg after I/R. The sham group underwent surgery without ischemia and received the drug/AST solvent (5% DMSO) for seven days. The I/R group experienced 30 minutes of ischemia followed by seven days of treatment with the drug solvent. The AST-treated groups (AST 5, 10, and 15 mg/kg) were subjected to the same ischemic conditions and subsequently received their respective doses of AST. After the treatment period, kidney tissues were harvested for histological examination, and serum samples were analyzed for renal function markers (urea and creatinine) and oxidative/antioxidant biomarkers, including catalase, glutathione (GSH), and nitrite. Results: The results indicated that AST administration significantly alleviated the detrimental effects of I/R injury in the rat model. Biochemical analysis revealed marked reductions in serum levels of urea and creatinine, alongside increases in antioxidant levels (catalase and GSH) and decreases in nitrite levels in the AST-treated groups. Notably, rats receiving AST exhibited a substantial reduction in renal tissue damage. Conclusions: The AST demonstrated significant protective effects against I/R injury in the rat model, as evidenced by improvements in kidney function, histology, and serum antioxidant biomarker profiles.