血糖波动抑制人脐静脉内皮细胞增殖能力的机制研究  

Fluctuating glucose inhibit human umbilical vein endothelial cells' proliferation and its Mechanisms

作　　者：姚瑶[1] 应长江[2] 周冬梅[2] 李伟[2] 

机构地区：[1]徐州医学院研究生学院,江苏徐州221000 [2]徐州医学院附属医院,江苏徐州221000

出　　处：《基层医学论坛》2015年第22期3030-3033,共4页The Medical Forum

基　　金：徐州市社会发展项目(K C 14S H 094)

摘　　要：目的研究血糖波动对人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)增殖能力的影响及其作用机制。方法体外培养HUVEC并用不同浓度葡萄糖进行处理,采用细胞增殖试剂盒(Cell Counting Kit-8,CCK8)法检测HUVEC增殖能力;Westernblot法检测蛋白激酶B(protein kinase B,Akt)蛋白、磷酸化蛋白激酶B(Phosphorylated protein kinase B,p-Akt)蛋白表达水平。结果与正常对照组比较,高糖可抑制HUVEC的增殖能力及p-Akt蛋白表达水平(P<0.05),血糖波动进一步加剧这一抑制作用(P<0.05)。应用磷脂酰肌醇3磷酸激酶(Phosphatidylinositol 3 phospho kinase,PI3K)抑制剂LY294002干预后,HUVECs的增殖能力及p-Akt蛋白表达水平较正常对照组降低(P<0.05)。结论血糖波动可能通过抑制磷脂酰肌醇3磷酸激酶/蛋白激酶B(Phosphatidylinositol 3 phospho kinase/proteinkinase B,PI3K/Akt)信号通路削弱人脐静脉内皮细胞增殖能力。ObjectiveTo investigate the effect of fluctuating glucose on the proliferation of human umbilical vein endothelial cells and explore its mechanisms.MethodsHUVEC were cultured in vitro and were treated in different concentrations of glucose.The proliferation of HUVEC was evaluated by CCK-8 method.The protein expressions of phospho-Ak and Akt were detected by Western blotting.ResultsHigh glucose inhibited the proliferation of HUVEC and the protein expression of phospho-Akt significantly compared with normal glucose group（P〈0.05）.Fluctuating glucose further exacerbate this inhibition（P〈0.05）.After treated with PI3Kt inhibitor LY294002,the proliferation of HUVECs and the protein expression of phospho-Akt was significantly decreased compared with normal glucose group（P〈0.05）.Conclusion Fluctuating glucose probably decreased the proliferation of HUVECs by inhibited the PI3K/Akt pathway.

关 键 词：血糖波动 人脐静脉内皮细胞 细胞增殖 PI3K/AKT信号通路 

分 类 号：R587.2[医药卫生—内分泌]