Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, China.
Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Purinergic Signal. 2019 Jun;15(2):193-204. doi: 10.1007/s11302-019-09655-4. Epub 2019 Jun 11.
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.
探讨腺苷外周受体在电针对炎症性肠病(IBD)小鼠内脏痛的影响中的作用。采用三硝基苯磺酸(TNBS)诱导内脏痛模型。TNBS 注射后 1 天,每日给予双侧“大肠俞”(BL25)穴位 1 mA、2 Hz、30 min 的电针治疗,连续 7 天。使用 von Frey 纤维测量机械痛阈值。Western blot 检测结肠组织中腺苷 A1 受体(A1R)、A2a 受体(A2aR)、A2b 受体(A2bR)、A3 受体(A3R)、P 物质(SP)和白细胞介素 1β(IL-1β)的蛋白表达水平。电针显著改善了疾病相关指标,并降低了 IBD 小鼠结肠组织中 SP 和 IL-1β的表达。电针增加了结肠组织中 A1R、A2aR 和 A3R 的表达,降低了 A2bR 的表达。此外,给予腺苷受体拮抗剂会影响电针的作用。电针可通过调节外周 A1、A2a、A2b 和 A3 受体来抑制炎症因子 SP 和 IL-1β的表达,从而抑制 IBD 小鼠的内脏痛。