Electroacupuncture inhibits visceral pain via adenosine receptors in mice with inflammatory bowel disease

• Published in: Purinergic signalling Vol. 15; no. 2; pp. 193 - 204
• Main Authors: Hou, Tengfei, Xiang, Hongchun, Yu, Lingling, Su, Wen, Shu, Yang, Li, Hongping, Zhu, He, Lin, Lixue, Hu, Xuefei, Liang, Shangdong, Zhang, Hong, Li, Man
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.06.2019; Springer Nature B.V
• Subjects: Acupuncture; Adenosine; Adenosine receptors; Animals; Biomedical and Life Sciences; Biomedicine; Cancer Research; Colon; Electroacupuncture; Filaments; Human Physiology; IL-1β; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory Bowel Diseases - metabolism; Interleukin 1; Intestine; Male; Mice; Neurosciences; Original; Original Article; Pain; Pharmacology/Toxicology; Receptors, Purinergic P1 - metabolism; Substance P; Sulfonic acid; Visceral Pain - metabolism; Visceral pain; Adenosine receptor; Inflammatory bowel disease (IBD); Electroacupuncture (EA)
• ISSN: 1573-9538; 1573-9546
• DOI: 10.1007/s11302-019-09655-4

To investigate the involvement of peripheral adenosine receptors in the effect of electroacupuncture (EA) on visceral pain in mice with inflammatory bowel disease (IBD). 2,4,6-Trinitrobenzene sulfonic acid (TNBS) was used to induce the visceral pain model. EA (1 mA, 2 Hz, 30 min) treatment was applied to bilateral acupoints “Dachangshu” (BL25) 1 day after TNBS injection once daily for 7 consecutive days. Von Frey filaments were used to measure the mechanical pain threshold. Western blot was used to detect the protein expression levels of adenosine 1 receptor (A1R), adenosine 2a receptor (A2aR), adenosine 2b receptor (A2bR), adenosine 3 receptor (A3R), substance P (SP), and interleukin 1 beta (IL-1β) in colon tissue. EA significantly ameliorated the disease-related indices and reduced the expression of SP and IL-1β in the colon tissues of mice with IBD. EA increased the expression of A1R, A2aR, and A3R and decreased the expression of A2bR in the colon tissue. Furthermore, the administration of adenosine receptor antagonists influenced the effect of EA. EA can inhibit the expression of the inflammatory factors SP and IL-1β by regulating peripheral A1, A2a, A2b, and A3 receptors, thus inhibiting visceral pain in IBD mice.