ABSTRACT
Objective To compare the pathological status of gastric mucosa and the expression of HH-PTCH-SMO-GLI(Hedgehog signaling pathway)and NOX/NF-κB/STAT1 signaling pathways in Hp and non-HP infected CAG patients,and to explore the biological mechanism of Hp promoting the"inflammatory cancer transformation"of CAG.Methods 43 patients with CAG who met the criteria were enrolled and divided into CAG with Hp infection group(Hp+ CAG group,n=21)and CAG without Hp infection group(HP-CAG group,n=22).The histological changes of gastric mucosa were observed by hematoxylin-eosin(HE)staining.Western blot was used to detect the relative expression levels of NOX1,NOX2,NOX4,STAT1,P65 and P-P65 in gastric mucosa.Real-time fluorescence quantitative PCR(RT-qPCR)was used to detect Gli1 mRNA,Gli2 mRNA,Gli3 mRNA,Shh mRNA,Smo mRNA,Ptch mRNA,NOX1 mRNA,NOX2 mRNA,NOX4 mRNA and NF-κB mRNA in gastric mucosa The mRNA level.Results HE staining results of gastric tissues in the two groups:In the Hp+CAG group,gastric epithelial cells were partially necrotic and shed,the surface was not smooth,the number of glands was reduced and disordered,intestinal metaplasia was observed,and diffuse lymphocyte and neutrophil infiltration were observed in the lamina proper.The degree of lymphocyte and neutrophil infiltration in HP-CAG group was lighter than that in Hp+CAG group.RT-qPCR results:Compared with HP-CAG group,the levels of Gli1 mRNA,Shh mRNA,Smo mRNA and Ptch mRNA in gastric mucosa of Hp+CAG group were significantly decreased(P<0.01).The levels of Gli2 mRNA,Gli3 mRNA,NOX1 mRNA,NOX2 mRNA,NOX4 mRNA and NF-κB mRNA were significantly increased(P<0.01).Western blot detection results:Compared with hP-CAG group,the relative expression levels of NOX1/GAPDH,NOX2/GAPDH,NOX4/GAPDH and P-P65/GAPDH in gastric mucosa of Hp+CAG group were significantly increased(P<0.01),and the STAT1 level was significantly decreased(P<0.01).There was no significant difference in the relative expression of P65/GAPDH between the two groups(P>0.05).Conclusion Hp infection may cause long-term inflammation of gastric mucosa,promote atrophy and intestinal metaplasia,and increase the risk of cancer by inhibiting hH-PTC-SMO-GLi signaling pathway and abnormal activation of NOX/NF-κB/STAT1 signaling pathway.