Display Settings:

Format

Send to:

Choose Destination
    World J Gastroenterol. 2004 Mar 1;10(5):682-8.

    Mechanisms of acupuncture and moxibustion in regulation of epithelial cell apoptosis in rat ulcerative colitis.

    Source

    Shanghai Institute of Acupuncture--Moxibustion and Meridians, Shanghai 200030, China. wuhuangan@citiz.net

    Abstract

    AIM:

    To investigate the effect of acupuncture and moxibustion on epithelial cell apoptosis and expression of Bcl-2, Bax, fas and FasL proteins in rat ulcerative colitis.

    METHODS:

    A rat model of ulcerative colitis was established by immunological methods and local stimulation. All rats were randomly divided into model control group (MC), electro-acupuncture group (EA), herbs-partition moxibustion group (HPM). Normal rats were used as normal control group (NC). Epithelial cell apoptosis and expression of Bcl-2, Bax, fas and FasL proteins were detected by TUNEL and immunohistochemical method respectively.

    RESULTS:

    The number of epithelial cell apoptosis in MC was significantly higher than that in NC, and was markedly decreased after the treatment with herbs-partition moxibustion or electro-acupuncture. The expression of Bcl-2, Bax, fas and FasL in colonic epithelial cells in MC was higher than that in NC, and was markedly down- regulated by herbs-partition moxibustion or electro-acupuncture treatment.

    CONCLUSION:

    The pathogenesis of ulcerative colitis in rats involves abnormality of apoptosis. Acupuncture and moxibustion can regulate the expression of Bcl-2, Bax, fas and FasL proteins and inhibit the apoptosis of epithelial cells of ulcerative colitis in rats by Bcl-2/Bax, fas/FasL pathways.

    PMID:
    14991938
    [PubMed - indexed for MEDLINE]
    Free full text

      Supplemental Content

      Icon for Baishideng Publishing Group Co., Limited

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk