Moxibustion inhibits apoptosis and tumor necrosis factor-alpha/tumor necrosis factor receptor 1 in the colonic epithelium of Crohn's disease model rats

Dig Dis Sci. 2012 Sep;57(9):2286-95. doi: 10.1007/s10620-012-2161-0. Epub 2012 Apr 25.

Abstract

Background: Previous studies have shown that moxibustion on Tianshu (ST25) and Qihai (CV6) is effective for treating Crohn's disease. However, the mechanism of moxibustion has not been clearly elucidated.

Aim: The purpose of this study was to investigate the effect of moxibustion on the inhibition of colonic epithelial cell apoptosis and on tumor necrosis factor alpha (TNF-alpha) and tumor necrosis factor receptor TNF receptor-1 (TNFR1) and TNFR2 and to determine the mechanism of its protective effect using Crohn's disease (CD) model rats.

Methods and results: The experimental CD rat models were established by the administration of trinitrobenzene sulfonic acid. In the herbs-partitioned moxibustion (HPM) and mild-warm moxibustion (MWM) groups, moxibustion was administered to Tianshu (ST25) and Qihai (CV6) acupoints once daily for 14 days. In the salicylazosulfapyridine (SASP) group, SASP was administered twice daily for 14 days. A normal control (NC) group and a model control (MC) group were also studied. The levels of TNF-alpha and its mRNA, TNFR1 as well as the rate of colonic epithelial cell apoptosis were significantly decreased in the HPM, MWM and SASP groups compared with the MC group. The HPM and MWM groups had lower mRNA expression and lower protein levels of TNF-alpha compared to the SASP group. The HPM and MWM groups exhibited less apoptosis than the SASP group.

Conclusions: Moxibustion may inhibit colonic epithelial cell apoptosis by reducing the high expression of TNF-alpha and TNFR1 to protect the defective colonic epithelial barrier in CD model rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Colon / metabolism*
  • Colon / pathology
  • Crohn Disease / therapy*
  • Flow Cytometry
  • Gene Expression Regulation
  • In Situ Nick-End Labeling
  • Intestinal Mucosa / metabolism*
  • Moxibustion / methods*
  • Rats
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Receptors, Tumor Necrosis Factor, Type I / genetics
  • Receptors, Tumor Necrosis Factor, Type I / metabolism*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Receptors, Tumor Necrosis Factor, Type I
  • Tnfrsf1a protein, rat
  • Tumor Necrosis Factor-alpha