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缺氧条件下新生大鼠皮质神经元凋亡的机制

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摘要 目的探讨Bcl-2家族促凋亡成员和抗凋亡成员对CoCl2诱导的新生大鼠皮质神经元缺血缺氧模型中神经元存活的影响及其调节机制。方法体外培养原代皮质神经元并建立CoCl2诱导大鼠皮质神经元缺血缺氧模型,用聚合酶链反应和Western免疫印迹技术,检测皮质神经元凋亡时Bcl-2家族促凋亡成员和抗凋亡成员的表达变化。结果促凋亡蛋白Bax在CoCl2模拟缺血缺氧时蛋白上调;而抗凋亡蛋白Bcl-2下降,总体蛋白水平下调(P<0.05)。结论 Bcl-2家族促凋亡成员Bax和抗凋亡成员Bcl-2比例的上升是缺血缺氧过程中神经元凋亡的关键因素。
作者 萧慧敏 杨秀芬 白文 李晓峰 苏浩彬
机构地区 东莞康华医院新生儿科 中山大学 中山大学孙逸仙纪念医院新生儿科
出处 《广东医学》 CAS CSCD 北大核心 2012年第6期754-756,共3页 Guangdong Medical Journal
关键词 缺血缺氧 皮质神经元 Bcl-2 BAX 凋亡
分类号 R743.35 [医药卫生—神经病学与精神病学]
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共引文献20

广东医学
2012年 第6期

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