| Aim To model chronic atrophic gastritis(CAG)rats,and observe the effect of Jianpi huayu jiedu decoction(JPHYJDD)on general conditions and histopathological changes of gastric mucosa of CAG rats.Moreover,we would explore the effect of JPHYJDD on the expression of p-Erk1/2 and Cyclin D1 in gastric epithelial cells of CAG rats.Method A total of 52 male SD rats were randomly divided into control group(n=10)and model group(n=42),and rats in the control group were fed routinely,while rats in the model group were free to 120μg·ml-11 MNNG solution everyday,and subject to hunger-satiety shift every other day,with the administration of 30%alcohol on the hunger day by gastrogavage to establish CAG rats model,during the modeling period,4 rats in the model group died.At end of the 8thh week,2 rats randomly selected from the model group were found to suffer the CAG lesion in the gastric mucosal tissue.At the 9thh week,except for the control group,rats in the remaining model group were randomly divided into model group(n=9),positive drug group(n=9),high-dose group of JPHYJDD(n=9)and low-dose group of JPHYJDD(n=9)to continue to drink 120μg·ml-11 of MNNG solution freely.At the same time,rats in each group were given corresponding drugs for 12 weeks,and control group and MNNG+model group were given normal saline 10ml·kg-1·d,MNNG+positive group was given folic acid 1.8mg·kg-1·d,MNNG+high dose group of JPHYJDD was given JPHYJDD 15.8g·kg-1·d,MNNG+low dose group of JPHYJDD was given JPHYJDD 7.9 g·kg-1·d.During the experiment,the general conditions of rats in each group was recorded,and their weight was monitored weekly,and after the experiment,gastric mucosal epithelial tissue specimens were prepared.The pathological changes of gastric mucosa were observed by HE staining,and the expression levels of p-Erk1/2 and Cyclin D1 protein in gastric epithelial cells were detected by immunohistochemistry.Data were processed by SPSS20.0 statistical software.Results 1.General conditions:the control group rats were in good mental state and the general situation was acceptable.The model group rats had mental retardation,decreased activity,severe depilation,decreased food and water intake,and the stool was not shaped.The general situation of each treatment group was improved.2.HE staining:In the control group,the glands of gastric mucosa epithelium were arranged normally,the cell structure was complete,the nucleus was regular and the nucleolus was obvious.In the MNNG+model group,the glands of gastric mucosa epithelium were arranged disorderly,the cell structure was incomplete,and the pathological signs such as nuclear hyperchromatism,nuclear pyknosis and nuclear dissolution were observed.The performance of atrophy of gastric mucosa,cell atypia and pathological mitosis of rats in each treatment group were improved in varying degrees.3.The expression of CyclinD1 in MNNG+model group was significantly increased compared with the control group(P<0.01).Compared with the MNNG+model group,the expression levels of CyclinD1 in all treatment group were significantly decreased(P<0.01 or P<0.05).Compared with the positive control group,the expression of CyclinD1 in MNNG+high dose group of JPHYJDD was significantly decreased(P<0.05).4.The expression of p-Erk1/2 of MNNG+model group increased significantly compared with the control group(P<0.01).Compared with the MNNG+model group,the expression of p-Erk1/2 in MNNG+high dose group of JPHYJDD decreased significantly(P<0.05),while the expression of p-Erk1/2 in positive control group and MNNG+low dose group of JPHYJDD decreased,but there was no significant difference(P>0.05).Compared with the positive control group,the expression of p-Erk1/2 in MNNG+high dose group of JPHYJDD was significantly decreased(P<0.05).Conclusion 1.JPHYJDD can effectively improve the general conditions and the histopathological changes such as glandular atrophy,disordered arrangement and dysplasia of gastric mucosa in CAG rats,and alleviate the development of CAG.2.There is high expression of p-Erk1/2 and CyclinD1 in CAG.JPHYJDD can down-regulate the expression levels of p-Erk1/2 and CyclinD1 in gastric epithelial cells of CAG rats.The mechanism may be related to the inhibition of Erk signal activation. |