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目的:探讨幽门螺杆菌热休克蛋白60(H.pylori-HSP60)感染胃上皮细胞后ERK与白介素-8(IL-8)分泌的关系。方法:利用ELISA技术,对活菌(IntactH.pylori)、死菌(Heat-killedH.pylori)及H.pylori-HSP60刺激胃上皮细胞KATOⅢ的IL-8蛋白分泌水平进行分析,观察IL-8随以上抗原浓度梯度的变化及ERK抑制剂PD98059对其分泌量的影响;利用Westernblot技术,观察KATOⅢ细胞中磷酸化ERK随IntactH.pylori、Heat-killedH.pylori及H.pylori-HSP60刺激时间的变化状况。结果:IL-8的分泌随着IntactH.pylori、Heat-killedH.pylori及H.pylori-HSP60刺激浓度的升高而增高;H.pylori刺激KATOⅢ细胞1h后ERK开始表达,其中IntactH.pylori在9h时表达达到高峰,Heat-killedH.pylori在24h时达到高峰,而H.pylori-HSP60刺激KATOⅢ细胞6h后ERK开始表达,9h时达到高峰;PD98059抑制了H.pylori-HSP60诱导的IL-8的分泌。结论:ERK介导了H.pylori-HSP60感染的胃上皮细胞的IL-8的分泌。
Objective: To investigate the relationship between ERK and interleukin-8 (IL-8) secretion in gastric epithelial cells infected with Helicobacter pylori heat shock protein 60 (H.pylori-HSP60). Methods: The levels of IL-8 in KATOⅢ of gastric epithelial cells stimulated by viable bacteria (H.pylori), killed-bacteriaH.pylori and H.pylori-HSP60 were analyzed by ELISA. And the effect of ERK inhibitor PD98059 on its secretion. Western blotting was used to observe the changes of phosphorylated ERK in KATOⅢ cells with time of Intact H.pylori, Heat-killed H.pylori and H.pylori-HSP60 . Results: The secretion of IL-8 increased with the increase of the concentration of IntactH.pylori, Heat-killedH.pylori and H.pylori-HSP60; The expression of ERK began to be expressed in KATOIII cells after 1 h of H.pylori stimulation, of which, IntactH.pylori was detected at 9h The expression of HSP70 reached its peak at 24 h, whereas the expression of ERK began to increase at 6 h after H.pylori-HSP60 stimulation, and peaked at 9 h. PD98059 inhibited the expression of IL-8 induced by H.pylori-HSP60 secretion. Conclusion: ERK mediates IL-8 secretion in H.pylori-HSP60-infected gastric epithelial cells.