Objective To observe the relatively specific effect of electroacupuncture(EA)of"Xiajuxu"(ST 39

the lower he-sea point of the small intestine)

etc.on the level of serum TNF-α

Interleukin-1β(IL-1β)and high mobility group protein B 1(HMGB 1)contents

and duodenumα7nicotinic acetylcholine receptor(nAchR)expression in duodenal ulcer rats

so as to explore its mechanisms underlying improving duodenal ulcer.Methods Sixty SD rats were randomly divided into 6groups:normal control

model

Xiajuxu(ST 39)

Zusanli(ST 36)

Shangjuxu(ST 37)and Yanglingquan(GB 34).The duodenal ulcer model was established by subcutaneous injection of 10% Cysteamine Hydrochloride(300mg/kg)

following by giving the rats with access to water containing Cysteamine.EA(10Hz/50 Hz

1-3mA)was applied to bilateral ST 39

ST 36

ST 37 and GB 34for30 min

once daily for 10 days.The ulcer scores(0-5points)of the duodenal mucosa were assessed according to modified Moraes' methods.Serum TNF-α

IL-1βand HMGB 1levels were assayed by ELISA and the expression of neuronalα7nAchR in the duodenal tissue was detected by Western blot.Results After modeling

the ulcer score

serum TNF-α

IL-1βand HMGB 1contents were significantly increased(P<0.01)and the expression level ofα7nAchR in the duodenal tissue was significantly downregulated in comparison with the normal control group(P<0.01).Following EA intervention

the serum TNF-αand HMGB 1contents in the Xiajuxu(ST 39)

Zusanli(ST 36)

Shangjuxu(ST 37)and Yanglingquan(GB 34)groups

and the ulcer scores and IL-1βcontent of the Xiajuxu(ST 39)

Zusanli(ST 36)and Shangjuxu(ST 37)groups were considerably reduced

and the expression ofα7nAchR in both Xiajuxu(ST 39)and Zusanli(ST 36)groups was evidently increased(P<0.05

P<0.01).No significant changes were found in the ulcer score

serum IL-1βcontent

andα7nAchR expression in the Yanglingquan(GB 34)group andα7nAchR expression in the Shangjuxu(ST 37)group in comparison with the model group(P>0.05).Conclusion EA stimulation of ST 36

ST 37 and ST 39 can reduce ulcer injury in duodenal ulcer model rats

which may be associated with their effects in down-regulating serum TNF-α

IL-1βand HMGB 1contents and up-regulatingα7nAchR expression of the duodenal tissue

possibly by suppressing immune and inflammatory reactions and regulating nicotinic activity.