This study is based on molecular docking and animal experiments to investigate the mechanism of Coptidis Rhizoma and Pinelliae Rhizoma in the treatment of chronic atrophic gastritis.First,the main components of Coptidis Rhizoma and Pinelliae Rhizoma were screened in the TCMSP database,and molecular docking was carried out with IL-1β,IL-6,YAP1,STAT3,JAK2,VEGF,and EGFR using vina software; Secondly,a compound method was used to establish a rat model,and the rats were randomly divided into model (B) group,vitrein (C) group,and low-,medium- and high-dose (D,E,F) groups,with 10 rats in each group.After successful modeling,groups D,E,and F were given HL and BX decoction (1∶2∶4) by gavage,respectively,and groups B and C were given NaCl (1 mL/100 g) and vermin,respectively.Groups were treated for a total of 8 weeks.After the treatment,the blood and gastric tissue samples of the rats were obtained,serum IL-1β and IL-6 levels were detected by ELISA.HE staining was used to observe the morphology of gastric tissue.RT-PCR detection of JAK2 mRNA,STAT3 mRNA,AKT1 mRNA,YAP1 mRNA,VEGF mRNA,EGFR mRNA expression in gastric tissue,the levels of p-STAT3,p-JAK2,p-AKT and p-YAP1 in gastric tissue were detected by WB.The experimental results found that the main active components of Coptidis Rhizoma and Pinelliae Rhizoma can bind to key targets; Each treatment group can effectively repair gastric mucosa morphology,reduce inflammation and intestinal metaplasia,and group E is better than other groups; The serum levels of IL-6 and IL-1β,the levels of JAK2 mRNA,STAT3 mRNA,AKT1 mRNA,YAP1 mRNA,VEGF mRNA,EGFR mRNA and the levels of p-STAT3,p-JAK2,and p-AKT1 in groups E and F were all in gastric tissue.It was significantly lower than that of group B and C (P<0.01).However,the level of p-YAP1 in each treatment group was significantly higher than that in group B (P<0.01),and group E was better than other groups.The experimental results show that the main components of Coptidis Rhizoma and Pinelliae Rhizoma can restore the morphology of gastric mucosa and prevent the evolution of malignant tumors by reducing the level of serum inflammatory factors in rats with chronic atrophic gastritis,inhibiting the JAK2/STAT3 pathway and angiogenesis pathway.