酰基化ghrelin通过PI3K/Akt通路抑制高糖诱导的内皮细胞凋亡

Acylated ghrelin inhibits high glucose-induced apoptosis in endothelial cells through PI3K/AKT pathway

目的研究酰基化ghrelin在高糖诱导的血管内皮细胞凋亡中的作用。方法通过Western-Blot、分光光度比色法分别检测Akt(Ser 473)磷酸化水平及caspase-3活性。结果 (1)不同浓度ghrelin(10^(-6)mol/L、10^(-7)mol/L)作用内皮细胞30min对Akt磷酸化作用的差异有统计学意义(P<0.05),而ghrelin(10^(-7)mol/L、10^(-8)mol/L、10^(-9)mol/L)浓度之间没有统计学差异(P>0.05),暴露于酰基化ghrelin(10^(-7)mol/L)中细胞内Akt迅速磷酸化,在30 min达高峰。(2)PI3K抑制剂LY294002可以减弱ghrelin对高糖(33.3mmol/L)环境下caspase-3活化的抑制作用。结论酰基化ghrelin通过PI3K/Akt通路抑制高糖诱导的内皮细胞凋亡,在糖尿病血管并发症的防治中可能有一定的意义。

Objective To investigate the role of acylated ghrelin in high glucose-induced apoptosis of ECV- 304 cells. Methods Western-blot and colorimetric assay were used. Results （1） Exposure of endothelial cells to acylated ghrelin （10^-7 M）rapidly caused activation of Akt, and the effect reached the peak at 30 min. A significant di（ference was observed in Akt phosphorylation level between 10^6 M and 10^-7 M ghrelin （P〈0. 05）, but there were no significant differences among different concentrations of acylated ghrelin （10^-7 M, 10^-8 M, 10^-9 M） （P〉0. 05）. （2） The inhibition effect of acylated ghrelin on caspase-3 activition under high glucose （33. 3 mM） was blocked by PI3K inhibitor （HG＋G： 1. 051 ±0. 014 HG＋ G＋Inhib： 1. 196±0. 041,P〈0. 05）. Conclusions Aeylated ghrelin inhibits high glucose-induced apoptosis in endothelial cells through PI3K/Akt pathway, and the peptide may have potential in preventing diabetic complications.