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为探讨丝裂原蛋白激酶(MAPK)和NF-κB信号通路在附睾上皮细胞炎症反应中的作用,以金黄色葡萄球菌(S.au-reus)感染附睾上皮细胞的体外感染模型,采用信号通路阻断剂、ELISA和Western blot等方法研究MAPK和NF-κB信号通路参与附睾上皮细胞的宿主防御。结果表明,附睾上皮细胞感染S.aureus后,诱导产生炎症因子TNF-α和IL-1,βNF-κB和p38 MAPK信号通路阻断剂BAY11-7082和SB203580能抑制S.aureus感染诱导的附睾上皮细胞炎症因子的产生。Western blot实验表明,附睾上皮细胞感染S.aureus后p38和IκB-α均被磷酸化,BAY11-7082和SB203580能分别抑制附睾上皮细胞感染S.aureus后p38和IκBα的磷酸化。表明p38 MAPK和NF-κB信号通路参与了S.aureus感染诱导的附睾上皮细胞炎症反应。
To investigate the role of mitogen-activated protein kinase (MAPK) and NF-κB signaling in the epididymal epithelial cell inflammatory response, in vitro infection of epididymal epithelial cells by S. aureus was investigated by using a signal pathway Blocking agents, ELISA and Western blot were used to study the host defense of epididymal epithelial cells by MAPK and NF-κB signaling pathway. The results showed that epididymal epithelial cells infected with S. aureus induced inflammatory factors TNF-α and IL-1, βNF-κB and p38 MAPK signal pathway blockers BAY11-7082 and SB203580 can inhibit S. aureus infection induced epididymal epithelium Production of cellular inflammatory cytokines. Western blot showed that both p38 and IκB-α were phosphorylated after epididymal epithelial cells were infected with S.aureus. The phosphorylation of p38 and IκBα was inhibited by BAY11-7082 and SB203580, respectively, after epididymal epithelial cells were infected with S. aureus. These results indicate that p38 MAPK and NF-|ÊB signaling pathways are involved in the inflammation of epididymal epithelial cells induced by S.aureus infection.