Protective effects of berberine in pancreatic islet beta cells
10.3969/j.issn.1000-4718.2014.12.017
- VernacularTitle:小檗碱对胰岛β细胞的保护作用及其机制研究
- Author:
Huiling WU
- Publication Type:Journal Article
- Keywords:
Berberine;
β-cells;
Apoptosis;
Insulin
- From:
Chinese Journal of Pathophysiology
2014;(12):2213-2218
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the protective effects of berberine (Ber) on islet beta cells and related possible mechanisms.METHODS:The injury of INS-1 cells was induced by treatment with alloxan ( Axn) .Berverine was then given at serial concentrations.The cells were divided into control group ( Con) , injury group ( Axn) , low-dose berberine group (LBer), medium-dose berberine group (MBer) and high-dose berberine group (HBer).Flow cytometry was em-ployed to detect the apoptosis.The activation of PTEN/PI3K/Akt and HNF-1α/PDX-1 pathways and the protein level of cleaved caspase-3 were evaluated by Western blotting.The insulin releases under normal or high-glucose stimulation were measured by ELISA.RESULTS:Compared with Con group, the apoptotic rate increased significantly in Axn group.Ber-berine treatment reduced the apoptotic rate in LBer group, MBer group and HBer group in a concentration-dependent man-ner.Compared with Con group, the protein levels of PTEN and cleaved caspase-3 increased, while PI3K and phosphoryla-tion of Akt decreased significantly in Axn group.However, this effect was reversed by berberine in a concentration-depend-ent manner.Compared with Con group, the activation of HNF-1α/PDX-1 signaling pathway was inhibited in Axn group but recovered by berberine administration.The abilities of releasing insulin under normal or high-glucose stimulation were im-paired in Axn group but recovered by berberine treatment in LBer group, MBer group and HBer group in a concentration-dependent manner.CONCLUSION:Berberine shows protective effects against alloxan-induced damage in beta cells by in-hibiting apoptosis and recovering insulin secretion, thus attenuating the activation of PTEN/PI3K/Akt and HNF-1α/PDX-1 signaling pathways.
