α-Hederin Mitigates Streptozotocin-induced Diabetic Nephropathy in Rats via Regulating Physiological Changes, Inflammation, and Oxidative Stress Responses

Background: Diabetic nephropathy, a severe microvascular complication of diabetes, is a primary cause of end-stage renal disease worldwide, significantly contributing to morbidity and mortality. Despite advancements in glycemic and blood pressure control, a substantial portion of diabetic patients still progress to diabetic nephropathy, underscoring the need for more effective therapeutic strategies. Objectives: The current work was devoted to examining the anti-diabetic nephropathy properties of α-hederin against streptozotocin (STZ)-induced rat model. Materials and Methods: The rats were treated with 65 mg/kg of STZ to develop diabetic nephropathy. The STZ-treated diabetic rats were subsequently administered α-hederin for a duration of 60 days. After the conclusion of treatments, body weight, blood glucose, kidney weight, and food and water consumption levels of the rats were examined. The levels of renal dysfunction markers, like uric acid, creatinine, and blood urea nitrogen, were determined. The levels of inflammatory cytokines and antioxidants were assessed using assay kits. Results: Treatment with 25 and 50 mg/kg of α-hederin significantly increased body weight and insulin levels and subsequently decreased glucose levels in rats with diabetic nephropathy. Moreover, α-hederin treatment reduced the levels of renal dysfunction markers in the serum of STZ-treated rats. The α-hederin treatment significantly decreased inflammatory cytokine levels and subsequently increased antioxidant levels in STZ-induced rats. Conclusion: The present data highlight that α-hederin may ameliorate diabetic nephropathy in the STZ-induced rat model. In conclusion, our findings indicate that α-hederin could serve as a beneficial therapeutic agent for diabetic nephropathy.