目的：研究线粒体PT孔(mitochondrial permeability transition pore, MPTP)在过氧化氢(hydrogen peroxide，H2O2)诱导的晶状体上皮细胞的凋亡中所起的作用。方法：家兔晶状体上皮细胞经不同浓度的环孢霉素A（线粒体PT孔专一性抑制剂）预处理30分钟，以阻断线粒体PT孔，再用0.1mmmol•L-1过氧化氢作用1小时后，分别用透射电镜观察细胞超微结构的改变，噻唑蓝法测定细胞线粒体的功能，流式细胞仪测定LECs的凋亡率变化。结果：过氧化氢诱导凋亡的晶状体上皮细胞，经不同浓度的环孢霉素A预处理后，较之无预处理组的细胞，其超微结构改变轻微，线粒体功能有不同程度的恢复，细胞凋亡率降低。并且这些改变表现出一定的环孢霉素A浓度依赖性。结论：线粒体PT孔参与了过氧化氢诱导的兔晶状体上皮细胞凋亡的调控；一定浓度的环孢霉素A可以抑制过氧化氢诱导的晶状体上皮细胞的损伤。

【Abstract】Objective To investigate the possible role of mitochondrial permeability transition pore( MPTP) in the control of the apoptosis of rabbit lens epithelial cells induced by hydrogen peroxide(H2O2). Methods In order to block the MPTP, rabbit lens epithelial cells have been pretreated with different concentration of cyclosporine A for 30 min, then 0.1mmol•L-1H2O2 was added and treated for 1 hour. Transmission electron microscope, MTT assay and flow cytometer were applied to detected the ultrastructure changes, the proliferation and the apoptosis percentage of the lens epithelial cells. Results Compared with the apoptosis cells without pretreatment of cyclosporine A, the cells that have been pretreated had less changes in ultrastructure and mitochondrial function and apoptosis rate. Conclusion Cyclosporine A can inhibit the damage to rabbit lens epithelial cells induced by hydrogen peroxide; Mitochondrial permeability transition pore play an important role in the control of the apoptosis of rabbit lens epithelial cells induced by hydrogen peroxide.