dehydroxymethylepoxyquinomicin has been researched along with Insulinoma* in 2 studies
2 other study(ies) available for dehydroxymethylepoxyquinomicin and Insulinoma
| Article | Year |
|---|---|
Inhibition of NO-induced β-cell death by novel NF-κB inhibitor (-)-DHMEQ via activation of Nrf2-ARE pathway.
Excessive nitric oxide (NO) plays a pivotal role in the progression of β-cell apoptosis in type 1 diabetes mellitus. We used mouse insulinoma Min6 cells as a model of β cells in this research. We found that (-)-DHMEQ, an NF-κB inhibitor, rescued β cells from NO-induced apoptosis, and then studied the mechanism of apoptosis inhibition. (-)-DHMEQ activated Nrf2 and induced transcription of Nrf2-target genes following the increase of antioxidant response element (ARE) reporter activity. Similarly, tert-butyl hydroquinone (tBHQ), a known activator of Nrf2, inhibited NO-induced cell death along with the transcriptional activation of ARE. RNAi-mediated knockdown of Nrf2 lowered the cytoprotective effect of (-)-DHMEQ against NO, suggesting that (-)-DHMEQ inhibited NO-induced cell death via Nrf2 activation. Furthermore, overexpression of Nrf2 rendered cells to be more resistant to NO, indicating that Nrf2 activation provides critical defense function against NO in Min6 cells. Taken together, we conclude that (-)-DHMEQ may be a useful therapeutic agent for type 1 diabetes mellitus in the onset of disease by protecting β cells from apoptosis. Topics: Animals; Antioxidant Response Elements; Apoptosis; Benzamides; Cyclohexanones; Gene Knockdown Techniques; Insulin-Secreting Cells; Insulinoma; Mice; NF-E2-Related Factor 2; NF-kappa B; Nitric Oxide; Pancreatic Neoplasms; Signal Transduction; Tumor Cells, Cultured | 2013 |
Effects of DHMEQ, a novel nuclear factor-kappab inhibitor, on beta cell dysfunction in INS-1 cells.
Recent studies suggest that nuclear factor-kappaB (NF-kappaB) 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-kappaB inhibitor, on tumor necrosis factor-alpha (TNF-alpha)-induced beta cell dysfunction.. INS-1 cells were incubated with TNF- alpha and with or without DHMEQ for 24 hours. Glucose-stimulated insulin secretion, cell viability, mRNA expression and NF-kappaB activation were investigated.. DHMEQ suppressed TNF-alpha-induced NF-kappaB 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-alpha.. DHMEQ suppressed NF-kappaB activation and ameliorated beta cell dysfunction induced by TNF- alpha. Inhibition of activated NF-kappaB in beta cells may be important to ameliorate beta cell dysfunction in diabetes. Topics: Animals; Benzamides; Cell Line, Tumor; Cell Survival; Cyclohexanones; Dose-Response Relationship, Drug; Glucose; Insulin; Insulin-Secreting Cells; Insulinoma; NF-kappa B; Pancreatic Neoplasms; Rats; Tumor Necrosis Factor-alpha | 2008 |