Notoginsenoside R1 alleviates TNF-α-induced pancreatic β-cell Min6 apoptosis and dysfunction through up-regulation of miR-29a

Diabetes mellitus (DM) is a metabolic disorder that seriously harms human health. Notoginsenoside R1 (NGR1) can be used in various diseases. We explored consequents of NGR1 on tumour necrosis factor (TNF)-alpha-stimulated Min6 and rat primary islets beta cells. The results were that TNF-alpha significantly cut down cell activity, raised cell apoptosis and iNOS expression and decreased insulin secretion in Min6 and rat primary islets beta cells. NGR1 alleviated TNF-alpha-treated cell dysfunctions. In addition, miR-29a was positively regulated by NGR1 in TNF-alpha-treated Min6 and rat primary islets beta cells. miR-29a knockdown damaged protection roles of NGR1 through cutting down cell activity and insulin secretion, raising apoptosis and iNOS in TNF-alpha-treated Min6 and rat primary islets beta cells. The phosphorylation of Wnt3a, beta-catenin and the rate of p/t-AKT/PI3K was all increased, while p/t-GSK3 beta was decreased by the administration with NGR1. In conclusion, NGR1 alleviated TNF-alpha-stimulated Min6 and rat primary islets beta cells apoptosis and worn roles via positively regulating miR-29a. This process might be through actuation of Wnt/beta-catenin and PI3K/AKT/GSK3 beta signal ways.