Tao Zhang, Fen Qiu
Department of Pharmacy, The Second Affiliated Hospital of Shandong University of Chinese Medicine, Jinan, Shandong, China (mainland)
Med Sci Monit 2020; 26:e924453
Available online: 2020-07-03
Type 2 diabetes (T2D) is characterized by ß-cell dysfunction and insulin resistance. Icariin (ICA), a flavonoid from Epimedium, possesses anti-diabetic and anti-inflammatory properties. However, it is unclear whether ICA acts on pancreatic ß-cells. The present study was designed to explore the effects and latent mechanism of ICA on uric acid (UA)-stimulated pancreatic b-cell dysfunction.
MATERIAL AND METHODS: Min6 cells were exposed to various concentrations of ICA for 24 h, and cell viability was assessed by MTT assays. Min6 cells were treated with ICA for 2 h, followed by 5 mg/dl UA for 24 h, and cell viability, apoptosis, apoptosis-associated protein levels and insulin secretion were assessed by MTT, flow cytometry, western blotting and glucose-stimulated insulin secretion assays, respectively. The effects of ICA and UA on the PI3K/Akt pathway were also analyzed by western blotting, as were the effects of the specific PI3K/Akt inhibitor LY294002.
RESULTS: ICA was not cytotoxic toward Min6 cells. UA decreased Min6 cell viability, enhanced cell apoptosis and levels of cleaved caspase-3, and reduced pro-caspase3 levels and insulin secretion, with all of these effects reversed by ICA in a dose-dependent manner. UA inhibited the PI3K/AKT pathway, an effect reversed by ICA treatment. The specific PI3K/Akt inhibitor LY294002, however, reversed these effects of ICA on UA-treated Min6 cells.
CONCLUSIONS: ICA protected Min6 cell function, an effect likely mediated by the PI3K pathway. ICA may inhibit the progression of diabetes.
Keywords: Diabetes Mellitus, Insulin-Secreting Cells, Phosphatidylinositol 3-Kinases