基于NF-κB信号通路Hp感染对胃癌小鼠炎症因子释放的促进作用  

Promoting effect of Hp infection on release of inflammatory factors in mice with gastric cancer based on NF-κB signal pathway

作　　者：贾纯亮[1] 梁磊[1] 张磊[1] 李翰嵩 王剑 刘远廷[1] JIA Chunliang;LIANG Lei;ZHANG Lei;LI Hansong;WANG Jian;LIU Yuanting(Department of Gastrointestinal Surgery,Tangshan Municipal People′s Hospital,Tangshan,Hebei 063000,China)

机构地区：[1]河北省唐山市人民医院胃肠外科,063000

出　　处：《重庆医学》2022年第1期34-40,共7页Chongqing medicine

基　　金：河北省医学科学研究课题计划项目(20201528)。

摘　　要：目的探讨幽门螺杆菌(Hp)感染小鼠致胃癌模型中核因子-κB(NF-κB)的活化情况及对炎症因子的影响。方法灌胃Hp菌液感染小鼠,并设对照组,分别于感染后18、36、54、72周采用酶联免疫吸附测定法检测血清白细胞介素-18(IL-18)、γ-干扰素(IFN-γ)、IL-10水平等;尿素酶试验及Giemsa染色观察Hp定植情况;苏木精-伊红染色观察胃黏膜病理学变化,并进行炎症评分;实时荧光定量聚合酶链反应(qRT-PCR)检测胃黏膜核苷酸结合寡聚化结构域1(NOD1)、受体相互作用蛋白2(RIP2)、NF-κB p65 mRNA表达;Western blot检测胃黏膜NOD1、RIP2、NF-κB p65、p-NF-κB p65蛋白表达。结果模型组小鼠各时间点Hp检测均为阳性,血清IL-18水平、IFN-γ水平,炎症评分,以及NOD1、RIP2 mRNA及蛋白、p-NF-κB p65蛋白表达水平均明显高于对照组,且随时间延长而升高,IL-10明显低于对照组,且随时间延长而降低,差异均有统计学意义(P<0.05)。结论NF-κB在Hp感染小鼠致胃癌模型中活化,并可促进炎症因子分泌,损伤胃黏膜。Objective To investigate the activation situation of nuclear transcription factor-κB(NF-κB)in the gastric cancer mouse model caused by Helicobacter pylori(Hp)infection and its influence on the inflammatory factors.Methods The Hp bacterial solution was gavaged to infect the mice,and the control group was set.Serum interleukin-18(IL-18)and interferon-γ(IFN-γ)and IL-10 levels were detected by ELISA in 18,36,54 and 72 weeks after infection,the urease test and Giemsa staining were used to observe the colonization of Hp,the HE staining was used to observe the pathological changes of gastric mucosa and the inflammation scoring was performed;qRT-PCR was used to detect nucleotide-binding oligomerization domain 1(NOD1),receptor interacting protein 2(RIP2),NF-κB p65 mRNA expression;Western blot was used to detect the expressions of gastric mucosal NOD1,RIP2,NF-κB p65 and p-NF-κB p65 protein.Results The Hp detection at each time point was positive in the model group,the expression levels of serum IL-18,IFN-γ,inflammation score,NOD1,RIP2 mRNA and protein,and p-NF-κB p65 protein in the model group were significantly higher than those in the control group,moreover increased with time extension,the level of IL-10 was significantly lower than that in the control group and decreased with time extension,and the differences were statistically significant(P<0.05).Conclusion NF-κB is activated in the mouse model of Hp infection,and can promote the secretion of inflammatory factors and damage the gastric mucosa.

关 键 词：胃肿瘤 幽门螺旋杆菌 核因子ΚB 炎症因子 信号通路 

分 类 号：R735.2[医药卫生—肿瘤]