ABSTRACT 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.
Vatanparast et al. (Thu,) studied this question.