Bilobalide alleviates tumor necrosis factor-alpha-induced pancreatic beta-cell MIN6 apoptosis and dysfunction through upregulation of miR-153.

Abstract

Type 1 diabetes mellitus (T1DM) is a systemic disease and one classical type of total DM. Bilobalide (BB) is constituted of EGb 761. Our purpose was identifying the role of BB in TIDM in the current study. MIN6 cells were treated by TNF-α; then, viability, apoptosis, and insulin secretion were assessed by performing Cell Counting Kit-8 assay, flow cytometry, glucose-stimulated insulin secretion assay, and western blot. The effects of BB were assessed to identify its function. Further, the above mentioned parameters were reassessed when silencing miR-153. TNF-α declined viability and insulin secretion as well as raised apoptosis and inducible nitric oxide synthase (iNOS) expression in MIN6 cells. BB alleviated the apoptosis and dysfunction induced by TNF-α. MiR-153 expression was elevated by BB when induced by TNF-α. Increase of viability and insulin secretion as well as decline of apoptosis and iNOS induced by BB treatment was alleviated by silencing miR-153. The rates of p/t-p70S6K, p/t-mammalian target of rapamycin (mTOR) and p/t-adenosine monophosphate-activated protein kinase (AMPK) were raised by BB and suppressed by silencing miR-153 under TNF-α induced condition. BB raised viability and insulin secretion, declined apoptosis and iNOS expression by up-regulating miR-153. Furthermore, BB activated AMPK/mTOR pathway by up-regulating miR-153.