Objective To observe the impact of catgut embedding on histopathological changes and expression of phosphorylated-Janus kinase-2(p-JAK 2)

phosphorylated-signal transducer and activator of transcription 3(p-STAT 3)

Cyclin D 1

Bcl-2

and suppressor of cytokine signaling(SOCS)of the gastric mucosa in chronic atrophic gastritis(CAG)rats

so as to explore its mechanisms underlying improving CAG.Methods Forty-one SD rats were randomly divided into normal(n=12)

model(n=9)

natural recovery(n=10)and catgut embedding(n=10)groups.The CAG model was established by free drinking of N-methyl-N'-nitro-N-nitroso-guanidine(MNNG)solution(100μg/mL)and irregular diet for 24 weeks.Catgut embedding was applied at bilateral"Zusanli"(ST 36)

"Pishu"(BL 20)and"Zhongwan"(CV 12)

once every 10 days

6 times altogether.The histopathological changes of the gastric mucosa were observed by naked eye and light microscope after H.E.staining.Wes-tern blot was used to detect the expression of p-JAK 2

p-STAT 3

CyclinD 1

Bcl-2 and SOCS 3 proteins in the gastric antrum tissue.Results After modeling

the regional gastric tissue showed pale thinner gastric wall

and poorer elasticity with fewer plica

congestion of blood vessels

reduction of regional glands with necrosis and disordered arrangement as well as evident hyperplasia of the connective tissue

which was evidently milder in the catgut embedding group.Compared with the normal group

the expression levels of p-JAK 2

p-STAT 3

CyclinD 1

Bcl-2

SOCS 3 proteins were significantly up-regulated in both model group and natural recovery group(P<0.01)

without significant differences between the latter two groups(P>0.05).After catgut embedding intervention

the expression levels of p-JAK 2

p-STAT 3

Cyclin D 1

Bcl-2 proteins were considerably down-regulated(P<0.01)

and that of SOCS 3 protein was notably further increased relevant to the natural recovery group(P<0.01).Conclusion Catgut embedding may improve pathological changes of gastric mucosa in CAG rats

which possibly associated with its effects in up-regulating gastric SOCS 3 protein expression and in inhibiting the activation of JAK 2-STAT 3 signaling pathway to reduce the expression of CyclinD 1 and Bcl-2 proteins.