Electroacupuncture reduced airway inflammation by activating somatosensory-sympathetic pathways in allergic asthmatic rats.
10.1097/CM9.0000000000003074
- Author:
Hongli MA
1
;
Xiaowen LIU
;
Huamei CAI
;
Yun YAN
;
Weixia LI
;
Jing ZHAO
Author Information
1. Department of Anesthesia, China-Japan Friendship Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100029, China.
- Publication Type:Journal Article
- MeSH:
Electroacupuncture/methods*;
Animals;
Asthma/immunology*;
Rats;
Rats, Sprague-Dawley;
Male;
Inflammation/therapy*;
Interleukin-4/metabolism*;
Interleukin-5/metabolism*
- From:
Chinese Medical Journal
2025;138(6):702-712
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:Electroacupuncture (EA) treatment is efficacious in patients with respiratory disorders, although the mechanisms of its action in lung-function protection are poorly understood. This study aimed to explore the neuroanatomical mechanisms of EA stimulation at the BL13 acupoint (Feishu, EA-BL13) improvement in asthma.
METHODS:Allergic asthma was induced by intranasal 2.0% ovalbumin (OVA) instillation combined with intraperitoneal injection of the 10.0% OVA. The levels of interleukin (IL)-4 and IL-5 were detected by enzyme-linked immunosorbent assay. Hematoxylin and eosin and periodic acid-schiff stain were used to evaluate inflammatory cell infiltration and mucus secretion. Cellular oncogene fos induction in neurons after EA stimulation was detected by immunofluorescent staining. The messenger RNA expression levels of adrenergic receptors were quantified with real-time polymerase chain reaction.
RESULTS:EA improved airway inflammation and mucus secretion mainly by activating somatosensory-sympathetic pathways ( P <0.001). Briefly, the intermediolateral (IML) nuclei of the spinal cord received signals from somatic EA stimulation and then delivered the information via the sympathetic trunk to the lung. Excited sympathetic nerve endings in lung tissue released large amounts of catecholamines that specifically activated the β2 adrenergic receptor (β2AR) on T cells ( P <0.01) and further decreased the levels of IL-4 and IL-5 ( P <0.001) through the cyclic adenosine monophosphate/protein kinase A signaling pathway.
CONCLUSION:This study provided a new explanation and clinical basis for the use of EA-BL13 as a treatment for allergic asthma in both the attack and remission stages and other respiratory disorders related to airway inflammation.
