【摘要】 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。更多还原

【Abstract】 To investigate the roles of the mitogen-activated protein kinase(MAPK) p38 and the nuclear factor kappa B(NF-κB) signal pathways on the inflammatory responses of epididymal epithelial cells induced by Staphylococcus aureus,rat epididymal epithelial cells in primary cultures were infected by S.aureus with or without the presence of NF-κB inhibitor BAY11-7082 and MAPK p38 inhibitors SP60025,SB203580 and PD98059 respectively.The levels of TNF-α and IL-1β in the supernatants of cell cultures were measured by ELISA and the phosphorylation of NF-κB and MAPK p38 was assessed at different times by Western blot analysis.It was found that the epididymal epithelial cells infected with S.aureus secreted significant amount of TNF-α and IL-1β in the supernatants of cell cultures.and NF-κB inhibitor BAY11-7082 inhibited completely secretion,while,MAPK p38 inhibitor SB203560 partly inhibited the secretion of these cytokines.As demonstrated by Western blot analysis,MAPK p38 and IκB-α in the infected cells could be phosphorylated.With these results,it is evident that p38 MAPK and NF-κB signal pathways might participate in the inflammatory responses of the epididymal epithelial cells infected with S.aureus.更多还原