中文摘要：

目的探讨周期性张应变诱导体外培养的膝关节骨关节炎（osteoarthritis，OA）患者软骨细胞发生凋亡过程中的活性氧（reactive oxygen species，ROS）的作用机制。方法对受力组软骨细胞施加频率0．5Hz、强度20％延伸率的周期性张应变。对照组细胞的培养条件与受力组细胞一致，但不受力。N-乙酰半胱氨酸（NAC）和丁胱亚磺酰亚胺（BSO）干预组的软骨细胞在受力前分别使用NAC和BSO进行预处理。流式细胞术检测细胞凋广率，DcFH-DA为荧光探针检测细胞内ROS含量，分光光度法检测软骨细胞内caspase-9活性变化。结果0．5Hz、20％延伸率的周期性张应变可以刺激软骨细胞内ROS、caspase-9活性及细胞凋亡率显著升高（P〈0．05）。使用NAC和BSO抑制及升高细胞内ROS含量后，可以明显抑制及促进周期性张应变诱导的软骨细胞的caspase-9活性及细胞凋亡率（P〈0．05）。结论周期性张应变通过促进ROS生成，进而激活caspase-9介导膝关节OA患者软骨细胞发生凋亡。抑制ROS的生成可以减轻周期性张应变导致的软骨细胞凋亡。

英文摘要：

Objective To explore the mechanism of reactive oxygen species （ROS） generation on apoptosis of human osteoarthritic chondrocytes induced by cyclic stretch in vitro. Methods The human osteoarthritic chon- drocytes were subjected to cyclic stretch at the frequency of 0.5 Hz with 20% elongation. The chondrocytes with- out cyclic stretch were used as a control. ROS generation in chondrocytes was inhibited by the antioxidant, N-ac- etyI-L-cysteine （NAC） and potentiated by the glutathione depleter, DL-buthionine-[ S, R ]-sulfoximine （BSO）. Apoptosis was detected by flow cytometry. Intracellular ROS was detected using DCFH-DA and caspase-9 activi- ty was measured using spectrophotometry. Results The cyclic stretch at the frequency of 0.5 Hz with 20% elon- gation induced ROS generation, and activation of caspase-9 and apoptosis in human osteoarthritic chondrocytes were significantly increased （ P 〈 0.05）. The inhibition or potentiation of intracellular ROS by NAC or BSO could obviously inhibit or improve caspase-9 activity and apoptosis in chondrocytes under cyclic stretch （P 〈0.05）. Conclusions Cyclic stretch-induced apoptosis in human osteoarthritic chondrocytes is mediated by ROS genera-tion and activation of caspase-9. Suppression of ROS can prevent chondrocytes from apoptosis induced by cyclic stretch,