Activation Of NOD1-NF-κB Signal Pathway In Gastrics Of Mice Infected With Helicobacter Pylori

ObjectivesTo construct Helicobacter pylori infected C57BL/6mouse model, and then observethe activation of NOD1-NF-κB signal pathway in the gastric tissues, and study its rolein inflammatory response caused by H. pylori infection.Methods:6~8weeks old C57BL/6mice were randomly divided into control groups and H.pylori infection group, and were challenged with H. pylori or PBS for five times every48h, repectively.4weeks after challenge, some mice were sacrificed to isolate gastrictissue and culture for H. pylori to identify the infection was successful. The isolatedgastric tissue and blood of mice were used for the following studies:(1) Inflammatoryresponse in gastric tissue was observed by HE staining;(2) The mRNA levels ofNOD1and RIP2in gastric tissues were detected by RT-PCR;(3) Levels of IFN-β andIP-10in mice serum were assessed by ELISA;(4) Nuclear translocation of p65ingastric tissue was detected by Western blot.Results:(1) H. pylori infection model was successfully constructed and no mice were dead. Inthe control group, their gastric tissue structures were normal. H. pylori infectionelicits an inflammatory cell response, glands in gastric tissue were reduced or atrophicto some degree.(2) Compared with control group, the levels of IP-10and IFN-β increased in themodel group, and peaked at16weeks after H. pylori infection.(3) The mRNA expression level of NOD1was higher than control group between24~120h after H. pylori infection (P<0.05), and the highest level at48h, subsequentlythe expression level began to decrease. (4) The mRNA expression level of RIP2was up regulated after H. pylori wasadministrated, peaked at48h and declined after72h. However at120h, the expressionlevels rise again.(5) After H. pylori infection, the expression level of NF-κB p65was significantlyhigher than control group between24~120h but peaked at48h, subsequently theexpression level decreased gradually to the normal level at120h.Conclusion:(1) H. pylori infection can up regulate NOD1and RIP2gene expression, andincrease nuclear translocation of NF-κB. Suggesting that H. pylori infection was ableto activate the NOD1-NF-κB signal pathways.(2) The levels of IFN-β and IP-10increased in serum of mice after H. pylori infection.