【摘要】 为探讨缺氧复氧致原代培养的大鼠大脑皮质神经细胞凋亡中 ,Bax基因的表达及银杏叶提取物 (EGB)对其的调节作用 ,用胎龄 1 6～ 1 7dWistar大鼠的大脑皮质神经细胞进行原代分离培养。采用原位末端标记法 (TUNEL)透射电镜技术确立缺氧复氧神经细胞凋亡病理模型 ,并应用免疫组织化学方法显示缺氧复氧不同时间Bax基因的表达。结果 :缺氧复氧可以使大鼠大脑皮质神经细胞发生凋亡 ,随缺氧时间的延长 ,凋亡细胞数逐渐增多 ,至缺氧 8h ,复氧 1 8h达高峰 ,银杏叶提取物预保护可使凋亡细胞数减少 ;同时随着缺氧时间的延长 ,Bax基因表达逐渐增高 ,EGB可逆转缺氧复氧时Bax的表达。提示 :EGB对缺氧复氧时Bax的表达具有明显的抑制作用 ,这可能是EGB对抗缺氧复氧时胎鼠大脑皮质神经细胞发生凋亡的机制之一。更多还原

【Abstract】 The aim was to investigate the expression of Bax protein in the apoptosis of primary cultured rat cortical neurons following hypoxia/reoxygenation(H/R) and the protective role of extract gingo biloba (EGB). The cortical neurons of E16～17 d fetal rat was primarily cultured. The apoptosis model of primary cultured cortical neurons following H/R was established by using TUNEL staining and electromicroscopy. The expression of Bax protein was investigated with immunohistochemical method. H/R can cause apoptosis of primary cultured rat cortical neurons. The apoptosis cell increased with the time, reaching peak value at H 8R 18 ; EGB could decrease the percentage of apoptosis. The expression of Bax protein increased with hypoxia time, EGB could inverse the expression of Bax. Conclusion: EGB could significantly inhibit the expression of Bax. It may be one of the mechanisms of apoptosis.更多还原