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目的研究NLRP3炎症小体信号通路相关分子在幽门螺杆菌(H.pylori)感染C57BL/6小鼠胃组织和血清中的表达情况,初步探讨NLRP3炎症小体信号通路在H.pylori致病中的作用。方法将C57BL/6小鼠分为H.pylori感染组和PBS对照组,于感染后不同时间点处死小鼠,RT-PCR检测小鼠胃组织中NLRP3炎症小体和下游信号通路分子mRNA表达,Western blot法检测小鼠胃组织中caspase-1蛋白表达,ELISA测定小鼠血清中IL-1β、IL-18和IL-33含量。结果与对照组相比,H.pylori感染组小鼠胃黏膜均呈慢性炎症改变,且随时间延长,炎症程度逐渐加重。NLRP3炎症小体信号通路相关分子mRNA及caspase-1蛋白表达水平显著升高,血清中IL-1β、IL-18、IL-33的含量均显著增高。结论 H.pyori感染可以激活NLRP3炎症小体信号通路。
Objective To study the expression of NLRP3 inflammasome signaling pathway-related molecules in gastric tissue and serum of H.pylori-infected C57BL / 6 mice and to explore the role of NLRP3 inflammasome signaling pathway in the pathogenesis of H.pylori effect. Methods C57BL / 6 mice were divided into H.pylori infection group and PBS control group, and mice were sacrificed at different time points after infection. The mRNA expression of NLRP3 inflammasome and downstream signaling pathway molecules were detected by RT-PCR, Western blot was used to detect the expression of caspase-1 protein in mouse gastric tissue. ELISA was used to detect the levels of IL-1β, IL-18 and IL-33 in the serum of mice. Results Compared with the control group, gastric mucosa of H.pylori-infected mice showed chronic inflammatory changes, and with the passage of time, the degree of inflammation gradually increased. The expression of IL-1β, IL-18 and IL-33 in the NLRP3 inflammasome signaling pathway mRNA and caspase-1 protein expression were significantly increased. Conclusion H. pyori infection can activate NLRP3 inflammasome signal pathway.