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作 者:周帅[1] 蒋理[1] 程崇杰[1] 殷成[1] 熊学华[1] 唐爽[1] 孙晓川[1]
机构地区:[1]重庆医科大学附属第一医院神经外科,重庆400016
出 处:《第三军医大学学报》2012年第20期2067-2069,共3页Journal of Third Military Medical University
基 金:国家自然科学基金(30973087)~~
摘 要:目的探讨载脂蛋白E(apolipoprotein E,APOE)在星形胶质细胞缺氧性损伤中的作用及相关机制。方法①原代培养APOE基因敲除鼠、APOE基因野生鼠的星形胶质细胞,并分别予以缺氧6 h,流式细胞仪分别检测两组细胞早期凋亡率情况;②将培养成熟的APOE基因野生鼠的星形胶质细胞分为常氧组、缺氧组和干预组(缺氧+ERK抑制剂),分别予以缺氧组和干预组缺氧6 h,干预组在缺氧之前向培养基中加入ERK信号通路抑制剂U0126,Western blot法分别检测检测3组细胞APOE蛋白表达变化情况。结果①缺氧6 h后,APOE基因敲除鼠组星形胶质细胞早期凋亡率[(5.67±0.35)%]明显高于APOE基因野生鼠组[(2.77±0.24)%](P<0.05);②与常氧组、干预组相比较,缺氧组星形胶质细胞表达的APOE蛋白明显增加(P<0.05)。结论 APOE对星形胶质细胞缺氧性损伤具有保护作用,缺氧后星形胶质细胞APOE蛋白水平上调与ERK信号通路有关。Objective To determine the effects of apolipoprotein E(APOE) on the astrocytes after hypoxic injury.Methods Astrocytes were separated from wild type mice and APOE knockout mice.Hypoxic injury models were established by putting cells in the setting of hypoxia for 6 h.The early apoptosis rate of astrocytes was detected by flow cytometry.The astrocytes from wild type mice were divided into normoxia group,hypoxia group and hypoxia + ERK inhibitor U0126 group.The expression of APOE in the 3 groups of cells was detected by Western blotting.Results The early apoptosis of astrocytes from APOE knockout mice [(5.67 ± 0.35) %]was significantly higher than the cells from the wild type [(2.77 ± 0.24) %,P〈0.05].Compared to normoxia group and hypoxia + ERK inhibitor U0126 group,the expression of APOE was highest in hypoxia group.Conclusion APOE exerts a protective effect on hypoxic injury of astrocytes.Hypoxic injury triggers astrocytes to increasingly synthesize APOE,through the ERK signaling pathway.
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学] R363[医药卫生—基础医学]
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