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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。
AIM To investigate the role of acylated ghrelin in the apoptosis of vascular endothelial cells induced by high glucose. Methods The phosphorylation of Akt (Ser 473) and the activity of caspase-3 were detected by Western-Blot and spectrophotometry. Results (1) The phosphorylation of Akt at different concentrations of ghrelin (10 -6 mol / L, 10 -7 mol / L) for 30 min had statistical significance (P <0.05) ghrelin (10 -7 mol / L, 10 -8 mol / L, 10 -9 mol / L), there was no significant difference (P> 0.05) (10 ~ (-7) mol / L) intracellular Akt phosphorylation, reached a peak at 30 min. (2) PI3K inhibitor LY294002 can reduce the inhibitory effect of ghrelin on the activation of caspase-3 in high glucose (33.3mmol / L) environment. Conclusion The acylation of ghrelin inhibits the apoptosis of endothelial cells induced by high glucose through the PI3K / Akt pathway, which may be of significance in the prevention and treatment of diabetic vascular complications.