Calebin A mitigates oxidative stress and inflammation in diabetic nephropathy via Nrf2/HO-1 and NF-κB signaling pathways.
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.
DN was induced in C57BL/6 mice using streptozotocin (STZ). Diabetic mice were treated with calebin A, curcumin, or metformin for 6 weeks.
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.
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.
DN was induced in C57BL/6 mice using streptozotocin (STZ). Diabetic mice were treated with calebin A, curcumin, or metformin for 6 weeks.
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.
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.
Authors
Vatanparast Vatanparast, Aliyari Aliyari, Yazdi Yazdi, Alidadi Alidadi, Sokhanvar Sokhanvar, Karav Karav, Kesharwani Kesharwani, Hosseini Hosseini, Sahebkar Sahebkar
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