Calebin A mitigates oxidative stress and inflammation in diabetic nephropathy via Nrf2/HO-1 and NF-κB signaling pathways
Journal of Diabetes Investigation, cilt.17, sa.4, ss.588-598, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 17 Sayı: 4
- Basım Tarihi: 2026
- Doi Numarası: 10.1111/jdi.70267
- Dergi Adı: Journal of Diabetes Investigation
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Directory of Open Access Journals
- Sayfa Sayıları: ss.588-598
- Anahtar Kelimeler: Antioxidant, Diabetes, Turmeric
- Çanakkale Onsekiz Mart Üniversitesi Adresli: Evet
Özet
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.