Electroacupuncture alleviates intestinal inflammation and barrier dysfunction by activating dopamine in a rat model of intestinal ischaemia

Author:

Li Yumeng1,Xu Guochen2,Hu Sen34,Wu Hong1,Dai Yuelong5,Zhang Wenhua3,Tang Fubo6,Luo Hongmin7,Shi Xian8

Affiliation:

1. Department of Encephalopathy, Anyang Hospital of Traditional Chinese Medicine, Anyang, China

2. Out-Patient Department, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, China

3. Laboratory of Shock and Multiple Organ Dysfunction, Trauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, China

4. Research Center of Trauma Repair and Tissue Regeneration, Medical Innovation Research Department, Chinese PLA General Hospital, Beijing, China

5. Chinese People’s Armed Police Force Academy, Langfang, China

6. Chengdu Hospital of Sichuan Provincial Corps, Chinese People’s Armed Police Force, Chengdu, China

7. Department of Burns and Wound Repair Surgery, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou, China

8. Department of Acupuncture and Moxibustion, Chinese PLA General Hospital, Beijing, China

Abstract

Background To investigate whether the mechanism underlying the anti-inflammatory effects of electroacupuncture (EA) at ST36 involves dopamine (DA) and its receptor and whether it is mediated by the vagus nerve in a rat model of intestinal ischaemia-reperfusion (I/R) injury. Methods Rats were subjected to gut ischaemia for 30 min and then received EA for 30 min with or without abdominal vagotomy or intraperitoneal administration of butaclamol (D1 receptor antagonist) or spiperone (D2 receptor antagonist). Plasma levels of DA and tumour necrosis factor (TNF)-α were assessed 1 or 4 h after reperfusion. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) content in intestinal tissues were assessed using enzyme-linked immunosorbent assay (ELISA) kits. Intestinal tissue injury was assessed by observation of the pathological lesions and permeability to 4 kDa fluorescein isothiocyanate (FITC)-dextran. Results EA significantly increased levels of DA and lowered levels of TNF-α. EA also inhibited intestinal levels of MPO and MDA and intestinal tissue injury and decreased intestinal permeability to FITC-dextran. Abdominal vagotomy and intraperitoneal administration of butaclamol (but not spiperone) inhibited the effects of EA. Conclusion These findings suggest that EA at ST36 could attenuate intestinal I/R-induced inflammatory injury and that the underlying mechanism may involve EA-induced increases in levels of DA, mediated by the vagus nerve and D1 receptors.

Publisher

SAGE Publications

Subject

Clinical Neurology,Complementary and alternative medicine,General Medicine

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