Zhu Jun, Chen Xiao-Yi, Li Lian-Bo, Yu Xin-Tong, Zhou Yin, Yang Wen-Jia, Liu Zhen, Zhao Na, Fu Cong, Zhang Shu-Hui, Chen Yun-Fei
Laboratory Center of Medicine, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Department of Acupuncture and Moxibustion, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Acupunct Med. 2015 Aug;33(4):305-11. doi: 10.1136/acupmed-2014-010732. Epub 2015 May 15.
Imbalance between T-helper 17 (Th17) cells and regulatory T (Treg) cells is causally linked to the development of rheumatoid arthritis (RA). In this study, we tested the hypothesis that electroacupuncture (EA) confers therapeutic benefits in RA through activation of vasoactive intestinal peptide (VIP)-dependent signalling and restoration of the Th17/Treg cell balance.
A collagen-induced arthritis (CIA) model was induced in Sprague-Dawley rats by injection of bovine type II collagen in incomplete Freund's adjuvant on day 0 and day 7. Three days after the second injection, EA was given at acupuncture points GB39 and ST36 three times per week for 4 weeks. To block VIP signalling, [D-P-Cl-Phe(6)-Leu(17)]-VIP, a VIP receptor antagonist, was administered intraperitoneally 30 min before EA. Inflammatory and pathological responses in the joint were assessed. Synovial VIP receptor mRNA levels and Treg and Th17 cell frequencies in the spleen were determined.
EA significantly reduced the severity of CIA, as evidenced by reduced paw volumes, arthritis scores and inflammation scores. EA significantly increased mRNA expression of the VIP receptor VPAC1 and led to an elevation in CD4(+)FOXP3(+) Treg cell frequency and a reduction in CD4(+)IL17(+) Th17 cell frequency. Pre-injection of a VIP receptor antagonist significantly reversed EA-induced expansion of Treg cells, but did not alter the frequencies of Th17 cells.
EA exerts anti-inflammatory effects in a collagen-induced rat model of arthritis. These effects appear to be mediated through activation of VIP signalling and re-establishment of the Th17/Treg cell balance.
辅助性T细胞17（Th17）与调节性T（Treg）细胞之间的失衡与类风湿关节炎（RA）的发病有因果关系。在本研究中，我们验证了以下假说：电针（EA）通过激活血管活性肠肽（VIP）依赖的信号传导和恢复Th17/Treg细胞平衡，从而对RA产生治疗作用。
在第0天和第7天，通过在弗氏不完全佐剂中注射牛II型胶原，在Sprague-Dawley大鼠中诱导胶原诱导性关节炎（CIA）模型。第二次注射后3天，每周3次在GB39和ST36穴位给予电针，共4周。为阻断VIP信号传导，在电针前30分钟腹腔注射VIP受体拮抗剂[D-P-Cl-Phe(6)-Leu(17)]-VIP。评估关节中的炎症和病理反应。测定滑膜VIP受体mRNA水平以及脾脏中Treg和Th17细胞频率。
电针显著降低了CIA的严重程度，爪体积减小、关节炎评分和炎症评分降低证明了这一点。电针显著增加了VIP受体VPAC1的mRNA表达，并导致CD4(+)FOXP3(+) Treg细胞频率升高以及CD4(+)IL17(+) Th17细胞频率降低。预先注射VIP受体拮抗剂可显著逆转电针诱导的Treg细胞扩增，但不改变Th17细胞频率。
电针在胶原诱导的大鼠关节炎模型中发挥抗炎作用。这些作用似乎是通过激活VIP信号传导和重建Th17/Treg细胞平衡来介导的。
