4.3 Article

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress

期刊

ACUPUNCTURE IN MEDICINE
卷 39, 期 2, 页码 135-145

出版社

SAGE PUBLICATIONS LTD
DOI: 10.1177/0964528420920288

关键词

corticotrophin-releasing factor receptor; electroacupuncture; gastrointestinal movement; jejunal motility; stress

资金

  1. National Natural Science Foundation of China Research Grants [81202763]
  2. National Basic Research Program of China [2011CB505200]
  3. Fundamental Research Funds for the Central Public Welfare Research Institutes [zz12004, 201814009]

向作者/读者索取更多资源

This study demonstrated that electroacupuncture treatment can improve stress-induced jejunal motility disorder, potentially through down-regulation of CRFr2.
Background Central injection of corticotrophin-releasing factor (CRF) mimics the effect of stress on gastrointestinal (GI) responses, including inhibition of GI motility. This study was designed to explore the effects of electroacupuncture (EA) on disordered jejunal motility in a rat model of stress induced by intracisternal (IC) injection of CRF. Methods A stress model was established by IC injection of CRF in Sprague-Dawley rats. GI motility was evaluated by assessing gastric emptying (GE), gastrointestinal transit (GIT) and jejunal motility in vivo. EA was performed at ST36. The functional roles of CRF receptor subtype 1 and subtype 2 (CRFr1 and CRFr2) were examined by IC administration of the corresponding selective CRF antagonists. Protein expression of CRFr1 and CRFr2 in the hypothalamus and jejunum was detected by Western blotting. Results IC injection of CRF significantly inhibited GE, GIT and jejunal motility. EA treatment remarkably improved the disturbed GI motility. Intriguingly, the disordered jejunal motility induced by central CRF was abolished by IC injection of a selective CRFr2 antagonist, indicating the essential role of central CRFr2 in mediating the stress-induced jejunal motor disorder. EA at ST36 decreased central and peripheral expression of CRFr2, which might be one of the potential mechanisms underlying the beneficial effect of EA on jejunal dysmotility in this rat model of stress. Conclusion This study suggested that EA at ST36 could ameliorate disordered jejunal motility induced by stress, and that this might be associated with the down-regulation of CRFr2.

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