摘要
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 apoptotie 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. Re- suits: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 o apoptosis of host cells involves activation of the MAPK/ERK signaling pathway.
出处
《激光生物学报》
CAS
CSCD
2012年第2期141-144,共4页
Acta Laser Biology Sinica