本文關鍵詞： 苗藥 黑骨藤 咖啡酰基奎寧酸類部位 人類風濕性關節(jié)炎成纖維樣滑膜細胞MHA 炎癥因子　出處：《中國藥房》2017年28期 　論文類型：期刊論文

【摘要】：目的:研究苗藥黑骨藤中咖啡酰基奎寧酸類部位(CADF)對腫瘤壞死因子α(TNF-α)誘導的人類風濕性關節(jié)炎(RA)成纖維樣滑膜細胞MH7A增殖及炎癥因子分泌的影響,探討CADF抗RA的作用機制。方法:將MH7A細胞分為空白組、TNF-α模型組、甲氨蝶呤組(陽性對照,20 mg/L)和CADF不同質量濃度組(50、100、200、400 mg/L),除空白組外,其余各組均以50μg/L TNF-α刺激活化MH7A細胞。以TNF-α與相應藥物的混合液共同作用24 h后,檢測細胞的增殖情況和培養(yǎng)液中一氧化氮(NO)、前列腺素E_2(PGE_2)、白細胞介素1β(IL-1β)、白細胞介素6(IL-6)的含量。結果:與空白組比較,TNF-α模型組細胞增殖活性顯著增強(P0.01),培養(yǎng)液中NO、PGE2、IL-1β、IL-6含量顯著增加(P0.01);與TNF-α模型組比較,各給藥組細胞的增殖均受到顯著抑制(P0.05或P0.01),培養(yǎng)液中NO、PGE2、IL-1β、IL-6含量均顯著減少(P0.01),且與CADF具有一定的量效關系。結論:CADF可通過抑制TNF-α誘導的MH7A細胞增殖,減少炎癥因子NO、PGE2、IL-1β、IL-6的分泌,從而發(fā)揮其抗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- 偽 (TNF- 偽). 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- 偽 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- 偽 model group was significantly increased (P0.01), and NOPGE2IL-1 尾 IL-6 was found in the culture medium. Compared with TNF- 偽 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- 偽 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- 偽, and decrease the secretion of the inflammatory factor NOPGE2IL-1 尾 -IL-6. In order to play its role in anti-RA.
【作者單位】： 貴州醫(yī)科大學民族藥與中藥開發(fā)應用教育部工程研究中心/國家苗藥工程技術研究中心;貴州醫(yī)科大學藥學院;貴州醫(yī)科大學貴州省藥物制劑重點實驗室;
【基金】：國家自然科學基金資助項目(No.81460641,81660691) 貴州省優(yōu)秀青年科技人才培養(yǎng)對象專項資金項目(No.黔科合人字[2015]11號) 貴州省科技計劃項目(No.黔科合平臺人才[2016]5677 黔科合平臺人才[2016]5613) 貴州省協(xié)同創(chuàng)新中心建設項目(No.黔教合協(xié)同創(chuàng)新字[2013]04) 貴州省研究生卓越人才計劃項目(No.ZYRC2014012)
【分類號】：R29
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本文編號：1554277