title: Moxibustion treatment restoring the intestinal epithelium barrier in rats with Crohn's disease by down-regulating tumor necrosis factor alpha, tumor necrosis factor receptor 1, and tumor necrosis factor receptor 2.
abstract: OBJECTIVE
  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).
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Shanghai Institute of Acupuncture-Moxibustion and Meridians, Shanghai University of Traditional Chinese Medicine, Shanghai, 200030, China.
authors.forename: Yin
authors.initials: Y
authors.lastname: Shi
authors.forename: En-Hua
authors.initials: EH
authors.lastname: Zhou
authors.forename: Huan-Gan
authors.initials: HG
authors.lastname: Wu
authors.forename: Ci-Li
authors.initials: CL
authors.lastname: Zhou
authors.forename: Qian-Yao
authors.initials: QY
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Qi
mesh_terms: D000818:Animals; D002463:Cell Membrane Permeability / Q000502:physiology; D003424:Crohn Disease / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D004195:Disease Models, Animal; D015536:Down-Regulation; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology / Q000502:physiology; D008297:Male; D009071:Moxibustion; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000378:metabolism*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha