雌激素激活pi3k-akt通路抑制血管内皮细胞内质网 应激凋亡-estrogen activates pi3k - akt pathway to inhibit endoplasmic reticulum stress apoptosis in vascular endothelial cells.docxVIP

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雌激素激活pi3k-akt通路抑制血管内皮细胞内质网 应激凋亡-estrogen activates pi3k - akt pathway to inhibit endoplasmic reticulum stress apoptosis in vascular endothelial cells.docx

雌激素激活pi3k-akt通路抑制血管内皮细胞内质网 应激凋亡-estrogen activates pi3k - akt pathway to inhibit endoplasmic reticulum stress apoptosis in vascular endothelial cells

万方数据万方数据目 录中文摘要·······································································································1 英文摘要·······································································································3 英文缩写·······································································································5 研究论文 雌激素激活 PI3K-Akt 通路抑制血管内皮细胞内质网应激凋亡 前言······································································································7 材料与方法··························································································9 结果······································································································14 附图······································································································17 讨论······································································································23 结论······································································································26 参考文献······························································································27综述 雌激素防止动脉粥样硬化的机制探讨··········································31 致谢··············································································································41 个人简历······································································································42中 中 文 摘 要 PAGE 10万方数据 PAGE 10万方数据雌激素激活 PI3K-Akt 通路抑制血管内皮细胞内质网应激凋亡摘 要目 的 : 本 研 究 的 目 的 是 明 确 雌 激 素 对 内 质 网 应 激 (endoplasmic reticulum stress, ERS)及过度的 ERS 诱导的人脐静脉内皮细胞(human umbilical vein endothelial cell, HUVEC)凋亡的抑制作用,并进一步研究其 抑制作用的分子机制,以探讨雌激素对心血管的保护机制。方法:10μmol/l 的衣霉素 (Tunicamycin, TM) 诱导 HUVEC10 小时 或 2mmol/l 的二硫苏糖醇(Dithiothreitol, DTT)诱导 8 小时,以构建 ERS 模型。 通过检测葡萄糖调节蛋白 78(glucose regulated protein, GRP78)的表达,判 断是否构建成功。提前给予 10-8mol/l 的 17-β 雌二醇(17β-estradiol, E2)预处 理 1 小时,量化分析 GRP78 的变化,以探索 E2 对 ERS 的作用。分别用 TM/DTT 诱导 HUVEC 6 小时,Western blot 检测 ERS 的三 条主要信号通路蛋白,包括蛋白激酶 R 样内质网激酶(protein kinase R-li

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