Caspase-3抑制剂Ac-DEVD-CHO对氧化损伤诱导晶状体上皮细胞凋亡的防护作用

目的 探讨半胱氨酸天冬氨酸酶(caspase-3)及其抑制剂Ac-DEVD-CHO对过氧化氢(H2O2)诱导大鼠晶状体上皮细胞凋亡的影响，为进一步研究晶状体氧化损伤机制及其防护提供实验依据。方法 采用大鼠离体晶状体器官培养的方法，用Western blot法分析氧化损伤后晶状体上皮细胞内caspase-3蛋白酶活性，流式细胞AnnexlnV-PI双染色法定量检测caspase-3抑制剂Ac-DEVD-CHO对晶状体上皮细胞凋亡率的影响。结果 氧化损伤诱导晶状体上皮细胞凋亡过程中，细胞内caspase-3酶活性明显增强，caspase-3特异性抑制剂Ac-DEVD-CHO可有效降低晶状体上皮细胞凋亡率。结论 caspase-3蛋白酶在氧化损伤诱导晶状体上皮细胞凋亡过程中占有重要地位，caspase-3抑制剂Ac-DEVD-CHO可有效防护体外品状体上皮细胞氧化损伤。

Protection of apoptosis induced by oxidative injury by caspase-3 inhibitor Ac-DEVD-CHO in rat lens epithelial cell

Objective To investigate the effect of caspase-3 and its inhibitor Ac-DEVD-CHO on H202-induced apoptosis of rat lens epithelial cells in vitro. Methods Rat' s lenses were incubated in vitro. The activity of caspase-3 was analyzed by Western blot method. Annexin V-PI methods was used to detect the effect of caspase-3 inhibitor Ac-DEVD-CHO on H202 -induced apoptosis of rat lens epithelial cells. Results Caspase-3 activity increased during H2 02-induced rat lens epithelial cell apoptosis. Cell apoptosis could apparently be blocked by caspase-3 inhibitor Ac-DEVD-CHO. Conclusions The activation of caspase-3 plays an important role in the development of apoptosis in H202-treated lens epithelial cells. The caspase-3 inhibitor Ac-DEVD-CHO can effectively prevent lens epithelial cells from apoptosis caused by oxidative injury.