ABSTRACT
<p><b>OBJECTIVE</b>To dynamically observe the effects of electroacupuncture (EA) on repair of gastric mucosal lesion in rats with gastric ulcer, and to explore the time-effect relationship and molecular mechanism of EA for gastric ulcer.</p><p><b>METHODS</b>A total of 72 SD rats were randomly assigned to a normal group, a model group, a acupoint group and a sham acupoint group, and each group were further divided into a 1-day subgroup, a 4-day subgroup and a 7-day subgroup, 6 rats in each subgroup. The rat model of gastric ulcer was established by using intragastric administration of ethyl alcohol. The rats in the acupoint group were treated with EA at"Zusanli"(ST 36) and"Liangmen"(ST 21); the rats in the sham acupoint group were treated with EA at points 5 mm next to"Zusanli"(ST 36) and"Liangmen"(ST 21); the EA was given 30 min per treatment, once a day. The rats in the normal group and model group were treated with immobilization for 30 min per day, and no EA was given. PR-PCR method was applied to test the expression of proliferating cell nuclear antigen (PCNA) and substance P (SP); Western blot method was applied to test the expression of neurotensin (NT).</p><p><b>RESULTS</b>After 1-day treatment, the ulcer index in the model group was higher than that in the normal group (<0.01), and the expression of PCNA, SP and NT was decreased (<0.01, <0.05); compared with the model group and sham acupoint group, the ulcer index was decreased in the acupoint group (both <0.05), and the expression of PCNA and SP was up-regulated (all <0.05) while that of NT was up-regulated (both <0.01). After 4-day treatment, the ulcer index in the model group was reduced but still higher than that in the normal group (<0.05), and the expression of PCNA, SP and NT was up-regulated and higher than that in the normal group (all <0.01); the ulcer index in the acupoint group was similar to that in the normal group (>0.05), and the expression of PCNA and SP was lower than that in the model group (<0.01, <0.05), and the expression of NT was not significantly different from that in the model group (>0.05). After 7-day treatment, the differences of indexes above were not significant among the four groups (all >0.05).</p><p><b>CONCLUSION</b>EA at acupoints of stomach meridian has two-way regulation on PCNA and SP and improve the expression of NT in different pathological state of gastric ulcer, which could further improve the repair of gastric ulcer.</p>
ABSTRACT
BACKGROUND/AIMS: Although neurotensin (NT) stimulates colon motility and the passage of intestinal contents, the associated mechanism of action remains unclear. The objective of this study was to investigate the effects of NT on colon motility using isolated rat colon. METHODS: Intraluminal pressure was measured at both the proximal and distal portions of the isolated colon. An isolated rat colon was perfused with Krebs solution via the superior mesenteric artery. After stabilization, NT was administered in concentrations of 14, 28, 138 and 276 pM. After pretreatment with phentolamine, propranolol, hexamethonium, atropine or tetrodotoxin, NT was administered at a concentration of 276 pM, and then the intraluminal pressure was monitored. RESULTS: NT significantly increased colon motility at concentrations of 14, 28, 138, and 276 in the proximal colon (25.1+/-6.5%, 175.4+/-117.0%, 240.8+/-115.1% and 252.3+/-110.6%, respectively) and in the distal colon (35.6+/-11.8%, 97.5+/-35.1%, 132.7+/-36.7% and 212.1+/-75.2%, respectively). The stimulant effect of NT was more potent in the proximal colon, in a concentration-dependent manner (P<0.05). The stimulant effect of NT was significantly inhibited by atropine at both the proximal and distal colon and by tetrodotoxin at the proximal colon, but not by tetrodotoxin at the distal colon and not by propranolol, phentolamine, or hexamethonium at both the proximal and distal colon. CONCLUSIONS: NT increased colon motility at both the proximal and distal portions of the rat colon. The effects were more prominent at the proximal portion. The results of this study suggest that the stimulant action of NT may be mediated by local cholinergic muscarinic receptors.