Calebin A mitigates oxidative stress and inflammation in diabetic nephropathy via Nrf2/ HO ‐1 and NF ‐ κB signaling pathways

BACKGROUND: Diabetic nephropathy (DN) is a common and serious microvascular complication of diabetes mellitus, primarily driven by persistent hyperglycemia-induced oxidative stress and chronic inflammation. Calebin A, a naturally occurring noncurcuminoid compound, has shown promising antioxidant and anti-inflammatory effects in various disease models. This study aimed to evaluate the nephroprotective effects and underlying mechanisms of calebin A in an experimental model of DN. METHODS: DN was induced in C57BL/6 mice using streptozotocin (STZ). Diabetic mice were treated with calebin A, curcumin, or metformin for 6 weeks. RESULTS: Treatment with calebin A resulted in significant improvements in glycemic control, renal function, oxidative stress, inflammation, fibrosis, and renal histopathological alterations. Calebin A reduced oxidative stress and inflammation by activating the Nrf2 pathway and downregulating the NF-κB signaling pathway. Histological analyses supported these findings by demonstrating marked attenuation of STZ-induced renal damage following calebin A administration. CONCLUSION: These results highlight the multitargeted nephroprotective effects of calebin A in DN. Further long-term and clinically oriented studies are warranted to validate these effects in chronic disease settings.