Protective Effect of Biochanin A on the Diabetes-Induced Renal Damage

Objective: Angiogenesis and oxidative stress contribute to the pathogenesis of diabetic nephropathy (DN). The isoflavone biochanin A (BCA) has reported anti-inflammatory and antioxidant properties; we evaluated whether BCA modulates inflammatory and angiogenic markers in renal tissue of streptozotocin-induced diabetic rats. Materials and Methods: Thirty-six male Wistar rats (180– 200 g) were randomized into six groups (n = 6): non-diabetic control (vehicle), diabetic control (STZ 55 mg/kg, i.p.), and two diabetic groups treated with BCA (10 or 15 mg/kg; Oral). Treatments were administered for 42 days. On day 42 animals were sacrificed and blood and renal tissues collected. Renal VEGF, TNF-α, IL-1β, IL-6, IL-18, NF-κB, TGF-β, RAGE, CTGF, and MDA were measured by ELISA. Renal tissues evaluate histopathologically for mesangial expansion, cellularity, and angiogenesis. Results: BCA treatment reduced fasting blood glucose in diabetic rats and significantly decreased renal VEGF, TNF-α, and IL-1β concentrations versus diabetic controls (p < 0.05). No clear dose-response was observed between 10 and 15 mg/kg; other markers showed non-significant trends toward improvement. Conclusion/Discussion: BCA reduced key angiogenic and proinflammatory markers in diabetic rat kidney, suggesting potential nephroprotective effects; further studies are needed to define mechanisms, optimal dosing, and long-term safety. Keywords: biochanin A, diabetic nephropathy, angiogenesis, inflammation, Wistar rat