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Chinese journal of integrative medicine ; (12): 212-217, 2011.
Article in English | WPRIM | ID: wpr-308701

ABSTRACT

<p><b>OBJECTIVE</b>To investigate whether moxibustion regulates tumor necrosis factor alpha (TNF-α), tumor necrosis factor receptor 1 (TNFR1), and TNFR2 in the intestinal mucosa and to explore whether moxibustion could be used by means of this mechanism, to repair the intestinal epithelium barrier disruption in Crohn's disease (CD).</p><p><b>METHODS</b>The CD rat models were established by trinitrobenzene sulfonic acid (TNBs), randomly divided into a model control (MC) group, an herb-partition moxibustion (HPM) group, a mild-warm moxibustion (MWM) group, and a salicylazosulfapyridine (SASP) group, and all were compared with a normal control (NC) group. The HPM and MWM groups were treated by moxibustion at Tianshu (ST25) and Qihai (RN6) for 14 days, and the SASP group obtained the SASP solution orally for the same period of time. The intestinal epithelium morphology and TNF-α, TNFR1, and TNFR2 contents were observed by the transmission electron microscopy and enzyme linked immunosorbent assay.</p><p><b>RESULTS</b>The severity of morphological changes in CD intestinal epithelium was obviously improved, and the levels of TNF-α, TNFR1, and TNFR2 in the intestinal mucosa all significantly decreased in the HPM and MWM groups. However, there were no significant differences between the HPM and MWM groups.</p><p><b>CONCLUSION</b>The moxibustion therapies (HPM and MWM) could reduce intestinal inflammation and restore intestinal epithelium barrier disruption in CD, which might be due to down-regulating TNF-α, TNFR1, and TNFR2 in intestinal mucosa and improving intestinal epithelium morphology.</p>


Subject(s)
Animals , Male , Rats , Cell Membrane Permeability , Physiology , Crohn Disease , Metabolism , Pathology , Therapeutics , Disease Models, Animal , Down-Regulation , Intestinal Mucosa , Metabolism , Pathology , Physiology , Moxibustion , Rats, Sprague-Dawley , Receptors, Tumor Necrosis Factor, Type I , Metabolism , Receptors, Tumor Necrosis Factor, Type II , Metabolism , Tumor Necrosis Factor-alpha , Metabolism
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