Aims: Recent studies suggest that nuclear factor-κB (NF-κB) activation has an important role in leading to beta cell dysfunction in both type 1 and type 2 diabetes. In this study we tested this hypothesis by investigating the effects of dehydroxymethylepoxyquinomicin (DHMEQ), a novel NF-κB inhibitor, on tumor necrosis factor-α (TNF-α)-induced beta cell dysfunction. Methods: INS-1 cells were incubated with TNF-α and with or without DHMEQ for 24 hours. Glucose-stimulated insulin secretion, cell viability, mRNA expression and NF-?̂B activation were investigated. Results: DHMEQ suppressed TNF-α-induced NF-κB activation and partially ameliorated glucose-stimulated insulin secretion in a dose-dependent manner. DHMEQ also partially ameliorated decreased cell viability and insulin mRNA level induced by TNF-α. Conclusion: DHMEQ suppressed NF-κB activation and ameliorated beta cell dysfunction induced by TNF-α. Inhibition of activated NF-κB in beta cells may be important to ameliorate beta cell dysfunction in diabetes.
- Cell viability
- Glucose-stimulated insulin secretion
- INS-1 cells
- Nuclear factor-κB
- Tumor necrosis factor-α
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism