Geniposide improves insulin production and reduces apoptosis in high glucose-induced glucotoxic insulinoma cells
Geniposide improves insulin production and reduces apoptosis in high glucose-induced glucotoxic insulinoma cells
复制标题
京尼平苷可改善高糖诱导的糖毒性胰岛素瘤细胞的胰岛素产生并减少细胞凋亡
DOI：
10.1016/j.ejps.2017.03.038
复制
发表时间：
2017-12-15
影响因子：
4.6
通讯作者：
Tam, K. Y.
中科院分区：
文献类型：
--
作者：
Guo, L. X.;Liu, J. H.;Tam, K. Y.
Our previous work revealed that in the pancreatic beta cell line, geniposide modulated ATP production and glucosestimulated insulin secretion (GSIS) induced by the acute stimulation of high glucose concentration. However, the effects of geniposide on functional impairment and the mass of beta-cells exposed to elevated levels of glucose remains unknown. In the present study, impaired GSIS and restrained proliferation were observed in the prolonged culture of insulinoma INS-1 cells with 33 mM of glucose (high glucose). Our results indicate that the glucose-induced impairment of insulin release was significantly reverted by the inclusion of 1 or 10 mu M of geniposide. Moreover, induction of the phosphorylation of AMP-activated protein kinase (AMPK) was observed, which promoted the utilization of nutrient stores for energy production. AMPK phosphorylation was enhanced by an increased number of INS-1 cells, and the increased expression of AMPK downstream target heme oxygenase 1 (HO-1), under high glucose concentration. Furthermore, geniposide protected rat insulinoma cells from apoptosis in high-glucose concentrations. We have shown that these effects were associated with an increased apoptosis-related Bcl-2/BAX protein ratio. In conclusion, geniposide dose dependently improves beta-cell function and increases the proliferation of beta-cells exposed to prolonged hyperglycemia.
