摘要
目的研究氧自由基诱导豚鼠耳蜗微血管内皮细胞凋亡及其可能机制。方法以黄嘌呤氧化酶作用于黄嘌呤而产生氧自由基,不同浓度氧自由基作用于豚鼠耳蜗微血管内皮细胞,用流式细胞术检测凋亡细胞的百分比;用免疫细胞化学法检测Bax及Bcl-2蛋白表达;用RT-PCR方法检测Bax及Bcl-2 mRNA的表达。结果氧自由基作用后,与空白对照组相比,各个浓度的氧自由基作用组豚鼠耳蜗微血管内皮细胞凋亡率均明显升高(均P<0.01),同时,Bax mRNA及蛋白的表达均显著增强(P<0.05或P<0.01),Bcl-2 mRNA及蛋白的表达明显减弱(均P<0.01)。结论氧自由基可诱导豚鼠耳蜗微血管内皮细胞发生凋亡,其发生机制与其调节Bax/Bcl-2 mRNA及蛋白的表达有关。
Objective To study the effects of oxygen free radical （OFR） on apoptosis in cochlea microvascular endothelial cells of guinea pigs. Methods Effects of oxygen free radical on the apoptosis in cochlea microvascular endothelial cells of guinea pigs Were detected by FACS. The expression of Bcl-2, and Bax mRNA and proteins was observed by TR-PCR and immunocytochemistry respectively. Results Apoptosis rate in cochlea microvascular endothelial cells of guinea pigs cultured with oxygen free radical was significantly increased as compared with controls. Oxygen free radical could significantly increase the expression of Bax, and decrease the expression of Bcl-2. Conclusion Oxygen free radical may lead to apoptosis of cochlea microvascular endothelial cells of guinea pigs, and the mechanism is related to the changes in Bax/Bcl-2.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2009年第3期359-363,共5页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家杰出青年科学基金资助项目(No.39925035)
关键词
氧自由基
耳蜗
微血管内皮细胞
细胞凋亡
oxygen free radical
cochlea
microvascular endothelial cells
apoptosis
