苗药黑骨藤中咖啡酰基奎宁酸类部位对人类风湿性关节炎成纤维样滑膜细胞MH7A增殖及炎症因子分泌的影响

发布时间：2018-03-02 00:29

  本文关键词： 苗药 黑骨藤 咖啡酰基奎宁酸类部位 人类风湿性关节炎成纤维样滑膜细胞MHA 炎症因子　出处：《中国药房》2017年28期 　论文类型：期刊论文

【摘要】：目的:研究苗药黑骨藤中咖啡酰基奎宁酸类部位(CADF)对肿瘤坏死因子α(TNF-α)诱导的人类风湿性关节炎(RA)成纤维样滑膜细胞MH7A增殖及炎症因子分泌的影响,探讨CADF抗RA的作用机制。方法:将MH7A细胞分为空白组、TNF-α模型组、甲氨蝶呤组(阳性对照,20 mg/L)和CADF不同质量浓度组(50、100、200、400 mg/L),除空白组外,其余各组均以50μg/L TNF-α刺激活化MH7A细胞。以TNF-α与相应药物的混合液共同作用24 h后,检测细胞的增殖情况和培养液中一氧化氮(NO)、前列腺素E_2(PGE_2)、白细胞介素1β(IL-1β)、白细胞介素6(IL-6)的含量。结果:与空白组比较,TNF-α模型组细胞增殖活性显著增强(P0.01),培养液中NO、PGE2、IL-1β、IL-6含量显著增加(P0.01);与TNF-α模型组比较,各给药组细胞的增殖均受到显著抑制(P0.05或P0.01),培养液中NO、PGE2、IL-1β、IL-6含量均显著减少(P0.01),且与CADF具有一定的量效关系。结论:CADF可通过抑制TNF-α诱导的MH7A细胞增殖,减少炎症因子NO、PGE2、IL-1β、IL-6的分泌,从而发挥其抗RA的作用。
[Abstract]:Aim: to study the effects of caffeyl quininic acid (CADF) in the seedling of Acanthopsis nigra on MH7A proliferation and inflammatory factor secretion in fibroblast of human rheumatoid arthritis (RA) induced by tumor necrosis factor- 伪 (TNF- 伪). Methods: CADF cells were divided into three groups: the blank group, the control group (20 mg / L) and the CADF group (50 mg / L), with the exception of the blank group, the control group and the control group. The other groups were stimulated with 50 渭 g / L TNF- 伪 to activate MH7A cells. The proliferation of cells and the contents of nitric oxide (no), prostaglandin E _ 2C (PGE2P), interleukin-1 (IL-1 尾), interleukin-6 (IL-6) in the culture medium were determined. Results: compared with the control group, the proliferation activity of the TNF- 伪 model group was significantly increased (P0.01), and NOPGE2IL-1 尾 IL-6 was found in the culture medium. Compared with TNF- 伪 model group, The proliferation of MH7A cells was significantly inhibited by P0.01G or P0.01G, and the content of IL-1 尾 IL-6 in the culture medium decreased significantly, and had a dose-effect relationship with CADF. Conclusion: VCADF can inhibit the proliferation of MH7A cells induced by TNF- 伪 and decrease the secretion of the inflammatory factor NOPGE2IL-1 尾 -guan6, which may be related to the proliferation of MH7A cells induced by TNF- 伪, and decrease the secretion of the inflammatory factor NOPGE2IL-1 尾 -IL-6. In order to play its role in anti-RA.
【作者单位】： 贵州医科大学民族药与中药开发应用教育部工程研究中心/国家苗药工程技术研究中心;贵州医科大学药学院;贵州医科大学贵州省药物制剂重点实验室;
【基金】：国家自然科学基金资助项目(No.81460641,81660691) 贵州省优秀青年科技人才培养对象专项资金项目(No.黔科合人字[2015]11号) 贵州省科技计划项目(No.黔科合平台人才[2016]5677 黔科合平台人才[2016]5613) 贵州省协同创新中心建设项目(No.黔教合协同创新字[2013]04) 贵州省研究生卓越人才计划项目(No.ZYRC2014012)
【分类号】：R29
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