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作 者:邢洁[1] 姜萍[1] 姜月华[2] 庞爱梅[2] 牟亮亮 梁占强[1] 张泽 秦林[1] XING Jie;JIANG Ping;JIANG Yue-hua;PANG Ai-mei;MU Liang-liang;LIANG Zhan-qiang;ZHANG Ze;QIN Lin(Shandong University of Chinese Medicine, Jinan 250014, China;Affiliated Hospital of Shandong University of Chinese Medicine, Jinan 250011, China)
机构地区:[1]山东中医药大学,济南250014 [2]山东中医药大学附属医院,济南250011
出 处:《中华中医药杂志》2018年第2期730-733,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:山东省科技发展计划项目(No.2014GSF119017)~~
摘 要:目的:探讨和痹方(HBR)通过胆碱能抗炎通路(CAP)治疗类风湿关节炎(RA)的机制。方法:将60只雄性大鼠随机平均分为空白组、模型组、激动剂组、HBR组、甲氨蝶呤(MTX)组、HBR+MTX组,激动剂组药物干预4周,其余组药物干预60d后,取血与关节滑膜,分别检测关节肿胀、肿瘤坏死因子α(TNF-α)、白介素(IL)-6、IL-17、α7烟碱型乙酰胆碱受体(α7nAChR)、转录激活因子3(STAT3)水平。结果:HBR组关节肿胀体积下降,α7nAChR、STAT3水平升高(P<0.05),TNF-α、IL-6、IL-17水平降低(P<0.01)。结论:HBR能够通过CAP,激活JAK2/STAT3信号通路,降低TNF-α、IL-6、IL-17水平,抑制炎性反应,减轻RA的关节肿胀。Objective:To investigate the mechanism of Hebi Recipe(HBR) by cholinergic anti inflammatory pathway(CAP) in the treatment of rheumatoid arthritis(RA).Methods:Sixty male rats were randomly divided into control group,model group,agonist group and HBR group,methotrexate(MTX) group,HBR+MTX group.The drug intervention in the agonist group was for 4 weeks,and the other groups were intervened for 60 days.Blood and joint synovial were taken to detect joint swelling,tumor necrosis factor-alpha(TNF-α),interleukin-6(IL-6),IL-17,alpha7 nicotinic acetylcholine receptor(α7 n ACh R) and activator of transcription3(STAT3) level.Results:The swelling volume of joint in HBR group decreased,the level of alpha 7nAChR and STAT3 increased(P〈0.05),and the level of TNF-α,IL-6 and IL-17 decreased(P〈0.01).Conclusion:HBR could activate JAK2/STAT3 signaling pathway through CAP,reduce the level of TNF-α,IL-6,IL-17,inhibit the inflammatory response,and reduce the swelling of the joint in RA.
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