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目的:探讨MAPK/ERK信号转导途径对鹦鹉热衣原体(Chlamydophila psittaci,Cps)感染细胞活性的影响。方法:利用化学抑制剂U0126阻断MAPK/ERK信号转导途径,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Cps感染细胞在凋亡诱导剂Etoposide作用下细胞凋亡率和Caspase-3活性和PARP裂解发生情况。结果:当MAPK/ERK信号通路被阻断时,在Etoposide的作用下,Cps感染细胞凋亡率明显提高,同时活化Caspase-3和促进PARP裂解。结论:Cps通过激活MAPK/ERK信号传导途径抑制宿主细胞凋亡活性。
Objective: To investigate the effect of MAPK / ERK signal transduction pathway on the cell activity of Chlamydophila psittaci (Cps) -infected cells. Methods: The MAPK / ERK signal transduction pathway was blocked by the chemical inhibitor U0126. Flow cytometry, Caspase-3 activity assay and Western Blot were used to detect the apoptosis of Cps-infected cells under the action of Etoposide Mortality and Caspase-3 activity and PARP cleavage. Results: When the MAPK / ERK signal pathway was blocked, the apoptosis rate of Cps-infected cells was significantly increased under the action of Etoposide, activating Caspase-3 and promoting PARP cleavage at the same time. Conclusion: Cps can inhibit the apoptosis of host cells by activating the MAPK / ERK signal transduction pathway.