Electroacupuncture ameliorates experimental colitis induced by acetic acid in rat.
- Author:
Jeoung Woo KANG
1
;
Tae Wan KIM
;
Jun Ho LA
;
Tae Sik SUNG
;
Hyun Ju KIM
;
Young Bae KWON
;
Jeum Yong KIM
;
Il Suk YANG
Author Information
1. Department of Physiology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea. isyang@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
colitis;
electroacupuncture;
glucocorticoid;
beta-adrenoceptor
- MeSH:
Acetic Acid;
Adrenergic beta-Antagonists/pharmacology;
Animals;
Carbachol/pharmacology;
Cholinergic Agonists/pharmacology;
Colitis/chemically induced/enzymology/pathology/*therapy;
Electroacupuncture/*veterinary;
Enzyme Inhibitors/metabolism;
Gastrointestinal Motility/physiology;
Hormone Antagonists/pharmacology;
Male;
Mifepristone/pharmacology;
Muscle Contraction/physiology;
Muscle, Smooth/drug effects/physiology;
NG-Nitroarginine Methyl Ester/pharmacology;
Peroxidase/metabolism;
Propranolol/pharmacology;
Rats;
Rats, Sprague-Dawley
- From:Journal of Veterinary Science
2004;5(3):189-195
- CountryRepublic of Korea
- Language:English
-
Abstract:
The effect of electroacupuncture (EA) on experimental colitis was investigated in Sprague-Dawley rats. Colitis was induced by intracolonic instillation of 4% acetic acid. EA (2 Hz, 0.05 ms, 2 V for 20min) was applied to bilateral Hoku (LI-4) and Zusanli (ST-36) on 12 hrs and 36 hrs after induction of colitis. EA-treatment significantly reduced the macroscopic damage and the myeloperoxidase activity of colonic samples at 3 days post-induction of colitis. Colitic colon showed a decreased in vitro motility. However, colonic motility of EAtreated group was not significantly different from that of normal group. The anti-inflammatory effect of EA was not inhibited by a glucocorticoid receptor antagonist, RU-486, but suppressed by a beta-adrenoceptor antagonist, propranonol. These results suggest that EA-treatment has a beneficial effect on colitis, and its anti-inflammatory effect is mediated by beta-adrenoceptor activation but not by endogenous glucocorticoiddependent mechanism.
