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: 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.
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Authors | Chun-Hui Bao, Lu-Yi Wu, Huan-Gan Wu, Yin Shi, Hui-Rong Liu, Rong Zhang, Li-Qing Yu, Jin-Hai Wang |
Journal | Digestive diseases and sciences
(Dig Dis Sci)
Vol. 57
Issue 9
Pg. 2286-95
(Sep 2012)
ISSN: 1573-2568 [Electronic] United States |
PMID | 22531889
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Receptors, Tumor Necrosis Factor, Type I
- Tnfrsf1a protein, rat
- Tumor Necrosis Factor-alpha
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Topics |
- Animals
- Apoptosis
- Colon
(metabolism, 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, metabolism)
- Tumor Necrosis Factor-alpha
(genetics, metabolism)
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