和痹方与甲氨蝶呤、艾拉莫德对胆碱能抗炎通路影响的比较研究  被引量:4

Comparation study on the influence of Hebi Formula,MTX and T-614 on CAP pathway

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作  者:马婷[1] 邢洁[1] 牟亮亮 梁占强 姜萍[1] MA Ting;XING Jie;MOU Liang-liang;LIANG Zhan-qiang;JIANG Ping(Shandong University of Traditional Chinese Medicine,Jinan 250014,China;Penglai Traditional Chinese Medicine Hospital,Penglai 265600,China;Shouguang Hospital of TCM,Shouguang 262700,China)

机构地区:[1]山东中医药大学,济南250014 [2]蓬莱市中医医院,蓬莱265600 [3]寿光市中医院,寿光262700

出  处:《中华中医药杂志》2021年第6期3594-3597,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:观察比较和痹方与艾拉莫德(T-614)、甲氨蝶呤(MTX)对类风湿关节炎(RA)胆碱能抗炎通路(CAP)的影响。方法:将通过手术获得的6例RA患者的膝关节无菌滑膜组织进行成纤维样滑膜细胞(FLS)的培养。分别用含有激动剂、MTX、T-614、和痹方、0.9%氯化钠溶液的药物血清刺激FLS。采用ELISA法观察滑膜细胞上清液中IL-17、HMGB1水平,采用Western Blot法检测滑膜细胞中α7nAChR、NF-κB p65、p-STAT3蛋白水平,RT-PCR法检测滑膜细胞中α7nAchR mRNA水平。结果:与模型组比较,MTX组、T-614组、和痹方组滑膜细胞中IL-17、HMGB1水平均显著降低(P<0.01,P<0.05)。MTX组、T-614组、和痹方组的NF-κB p65表达均显著降低(P<0.01,P<0.05),和痹方组α7nAChR、p-STAT3表达显著升高(P<0.05)。和痹方组α7nAChR mRNA的表达较MTX组、T-614组显著升高(P<0.05)。结论:和痹方能够通过上调α7nAChR mRNA、蛋白表达,激活CAP,调节NF-κB、JAK/STAT3信号通路,抑制炎症因子表达,而减轻炎症反应。Objective:To observe the effects of Hebi Formula and ilamomod(T-614)and methotrexate(MTX)on the cholinergic anti-inflammatory pathway(CAP)in rheumatoid arthritis(RA).Methods:The FLS culture of the knee joint sterile synovial tissue of 6 RA patients obtained by surgery was performed.FLS was stimulated with drug serum containing agonist,MTX,T-614,and sputum,physiological saline,respectively.The levels of IL-17 and HMGB1 in synovial cell supernatant were observed by ELISA.α7nAChR was detected by Western Blot in synovial cells.The levels of NF-κB p65,p-STAT3 were detected,and the level ofα7nAchR mRNA in synoviocytes was detected by RT-PCR.Results:Compared with the model group,the levels of IL-17 and HMGB1 in the MTX group,T-614 group and Hebi Formula group were lower(P<0.01,P<0.05).The expression of NF-κB p65 was decreased in MTX group,T-614 group and Hebi Formula group(P<0.01,P<0.05),α7nAChR and p-STAT3 expression in Hebi Formula group were increased(P<0.05).The expression ofα7nAChR mRNA in Hebi Formula group was significantly higher than that in MTX group and T-614 group(P<0.05).Conclusion:Hebi Formula can up-regulateα7nAChR mRNA,protein expression,activate CAP,regulate NF-κB,JAK/STAT3 signaling pathway,inhibit inflammatory cytokine expression,and reduce inflammatory response.

关 键 词:类风湿关节炎 成纤维样滑膜细胞 和痹方 Α7烟碱型乙酰胆碱受体 

分 类 号:R593.22[医药卫生—内科学]

 

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