Abstract
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)-α-stimulated Min6 and rat primary islets β cells. The results were that TNF-α significantly cut down cell activity, raised cell apoptosis and iNOS expression and decreased insulin secretion in Min6 and rat primary islets β cells. NGR1 alleviated TNF-α-treated cell dysfunctions. In addition, miR-29a was positively regulated by NGR1 in TNF-α-treated Min6 and rat primary islets β cells. miR-29a knockdown damaged protection roles of NGR1 through cutting down cell activity and insulin secretion, raising apoptosis and iNOS in TNF-α-treated Min6 and rat primary islets β cells. The phosphorylation of Wnt3a, β-catenin and the rate of p/t-AKT/PI3K was all increased, while p/t-GSK3β was decreased by the administration with NGR1. In conclusion, NGR1 alleviated TNF-α-stimulated Min6 and rat primary islets β cells apoptosis and worn roles via positively regulating miR-29a. This process might be through actuation of Wnt/β-catenin and PI3K/AKT/GSK3β signal ways.