RGD Reference Report - 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. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

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.

Authors: Shi, Y  Zhou, EH  Wu, HG  Zhou, CL  Wang, QY  Qi, L 
Citation: Shi Y, etal., Chin J Integr Med. 2011 Mar;17(3):212-7. Epub 2011 Feb 27.
RGD ID: 5130893
Pubmed: PMID:21359923   (View Abstract at PubMed)
DOI: DOI:10.1007/s11655-011-0669-3   (Journal Full-text)

OBJECTIVE: To investigate whether moxibustion regulates tumor necrosis factor alpha (TNF-alpha), 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-alpha, 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-alpha, 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. CONCLUSION: 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-alpha, TNFR1, and TNFR2 in intestinal mucosa and improving intestinal epithelium morphology.



1 to 9 of 9 rows

  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
TNFHumanCrohn's disease  ISOTnf (Rattus norvegicus)protein:increased expression:intestine mucosaRGD 
TNFRSF1AHumanCrohn's disease  ISOTnfrsf1a (Rattus norvegicus)protein:increased expression:large intestine mucosa (rat)RGD 
TNFRSF1BHumanCrohn's disease  ISOTnfrsf1b (Rattus norvegicus)protein:increased expression:large intestine mucosa (rat)RGD 
TnfRatCrohn's disease  IEP protein:increased expression:intestine mucosaRGD 
TnfMouseCrohn's disease  ISOTnf (Rattus norvegicus)protein:increased expression:intestine mucosaRGD 
Tnfrsf1aRatCrohn's disease  IEP protein:increased expression:large intestine mucosa (rat)RGD 
Tnfrsf1aMouseCrohn's disease  ISOTnfrsf1a (Rattus norvegicus)protein:increased expression:large intestine mucosa (rat)RGD 
Tnfrsf1bRatCrohn's disease  IEP protein:increased expression:large intestine mucosa (rat)RGD 
Tnfrsf1bMouseCrohn's disease  ISOTnfrsf1b (Rattus norvegicus)protein:increased expression:large intestine mucosa (rat)RGD 
1 to 9 of 9 rows


Genes (Rattus norvegicus)
Tnf  (tumor necrosis factor) Tnfrsf1a  (TNF receptor superfamily member 1A) Tnfrsf1b  (TNF receptor superfamily member 1B)

Genes (Mus musculus)
Tnf  (tumor necrosis factor) Tnfrsf1a  (tumor necrosis factor receptor superfamily, member 1a) Tnfrsf1b  (tumor necrosis factor receptor superfamily, member 1b)

Genes (Homo sapiens)
TNF  (tumor necrosis factor) TNFRSF1A  (TNF receptor superfamily member 1A) TNFRSF1B  (TNF receptor superfamily member 1B)