槲皮素调控PTEN-Akt通路抑制H_2O_2诱导的血管内皮细胞凋亡  

Quercetin Inhibiting H_2O_2 Induced-Apoptosis of Vascular Endothelial Cells by Regulating PTEN-Akt Pathway

作　　者：李跃艳[1] 全智华[1] 

机构地区：[1]南华大学附属第一医院心血管内科,湖南省衡阳市421001

出　　处：《中国动脉硬化杂志》2013年第12期1089-1092,共4页Chinese Journal of Arteriosclerosis

摘　　要：目的探讨槲皮素对人脐静脉内皮细胞(HUVEC)氧化应激损伤的保护作用及机制。方法通过H2O2作用于人脐静脉内皮细胞建立氧化应激模型,采用MTT法测定HUVEC细胞存活率,试剂盒法测定乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)活性,流式细胞术检测细胞周期,Western Blot法测定PTEN、Akt、磷酸化Akt及Bcl-2蛋白的表达水平。结果 H2O2可使HUVEC的存活率下降,而10、20μmol/L槲皮素处理后细胞存活率显著提高(P<0.05);SOD活性显著增加,而MDA与LDH水平显著降低(P<0.05),与H2O2处理组相比其细胞凋亡率明显降低,槲皮素能有效增加PTEN并减少p-Akt、Bcl-2的表达。结论中、高剂量槲皮素能有效保护HUVEC细胞使其免受H2O2的损害,该作用可能与其作用PTEN-Akt通路从而抑制内皮细胞凋亡有关。Aim To investigate protective effection of Quercetin （Que） on human umbilical vein endothelial cells （HUVEC） from oxidative stress injury in rats and its mechanism. Methods Oxidative stress model of HUVEC was established by H2O2. Then, MTT assay was used to investigate the cell proliferation ability. The content of lactate dehydrogenase （LDH）, malondialdehyde （MDA）, superoxide dismutase （SOD） were determinated by kits. Flow cytometry was used to detect cell apoptosis. The protein expression of PTEN, Akt, phospho-Akt and Bcl-2 were detected by Western Blot.Results H2O2 can decrease HUVEC survival, while 10, 20 μmol/L Que significantly increase cell viability （P〈0.05） Que treatment can significantly increase SOD activity, while significantly decrease MDA and LDH levels （P〈0.05）, and reduce their rate of apoptosis compared with H2O2 treatment group. Finally, Que can effectively increase PTEN and reduce p-Akt, Bcl-2 expression. Conclusion High-dose Que can effectively protect HUVEC cells against H2O2 damage this effect may be related to the role of PTEN-Akt pathway by inhibiting endothelial cell apoptosis.

关 键 词：槲皮素 氧化应激 内皮细胞 细胞凋亡 

分 类 号：R363[医药卫生—病理学]