目的: 研究沙眼衣原体抑制宿主细胞凋亡活性与MAPK/ERK信号通路的关系。方法: 利用化学抑制剂U0126阻断MAPK/ERK信号通路, 然后分别采用流式细胞术、Caspase-3活性检测试剂盒和Western Blot实验检测沙眼衣原体感染细胞在凋亡诱导剂Etoposide作用下细胞凋亡率和Caspase-3活性变化, 以及PARP是否发生裂解。结果: 当MAPK/ERK信号通路被阻断时, 在Etoposide的作用下, 沙眼衣原体感染细胞凋亡率明显上升, 同时Caspase-3被活化和PARP发生裂解。结论: 沙眼衣原体抑制宿主细胞凋亡活性与MAPK/ERK信号通路激活有关。

Objective: To investigate the relation between inhibition of apoptosis and MAPK/ERK signaling pathway in Chlamydia trachomatis-infected cells. Methods: MAPK/ERK signaling pathway was blocked by U0126 in Chlamydia trachomatis-infected cells, then the percentage of apoptotic cells, Capase-3 activity and PARP cleavage, which were induced by etoposide, were detected with flow cytometer, caspase-3 activity kit and Western Blot assay, respectively. Results: The percentage of apoptotic cells induced by etoposide was significantly higher, Caspase-3 was activated and PARP was cleft too, when MAPK/ERK signaling pathway was blocked by U0126. Conclusion: Chlamydia trachomatis inhibit apoptosis of host cells involves activation of the MAPK/ERK signaling pathway.