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European Review for Medical and Pharmacological Sciences 2013-Nov

The inhibitory effect of melatonin on colonic motility disorders induced by water avoidance stress in rats.

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W Tan
W Zhou
H-S Luo
C-B Liang
H Xia

Avainsanat

Abstrakti

OBJECTIVE

Psychological stress is involved in the etiology of functional gastrointestinal disease (FGID). Accumulations of chronic continuous stress associate with the symptoms of the gastrointestinal tract (GIT) including abdominal discomfort, pain, constipation or diarrhea. Melatonin (MT) is a neurohormone which mainly synthesized in the pineal gland and GIT, has been shown to alleviate the stress and regulate the intestinal motility. Although melatonin attenuated abnormal defecation induced by stress, the mechanisms of the effect are not fully elucidated. This study sought to investigate the effect of melatonin (MT) on colonic smooth muscle contractility disorders induced by chronic water avoidance stress (WAS).

METHODS

36 adult Wistar rats were divided into three groups [Control+V (vehicle solution), WAS+V, WAS+MT]. The WAS+V and WAS+MT groups were suffered from WAS for one hour daily for 10 days. Melatonin was given 30 min before stress session in the WAS+MT group. Colonic motility was assessed using the numbers of fecal pellet output. The concentrations of melatonin and serotonin (5-HT) were measured through ELISA method. The contractions of isolated colonic strips were assessed through isometric force transducer.

RESULTS

The numbers of fecal output was increased in the WAS+V group, and melatonin attenuates the increased fecal pellet output induced by WAS. The concentrations of 5-HT was increased by WAS, and melatonin decreased the augment in the concentration of 5-HT. In the part of contraction recording of colonic smooth muscle, melatonin inhibited the fortified spontaneous contraction induced by WAS, and decreased the amplitude of spontaneous contraction stimulated by Ach and KCl after WAS treatment.

CONCLUSIONS

Melatonin could inhibit WAS-induced fecal output pellets by inactivating the 5-HT pathway, may interact with calcium channel and inhibit the influx of calcium.

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