本文關(guān)鍵詞： 苗藥 黑骨藤 咖啡酰基奎寧酸類(lèi)部位 人類(lèi)風(fēng)濕性關(guān)節(jié)炎成纖維樣滑膜細(xì)胞MHA 炎癥因子　出處：《中國(guó)藥房》2017年28期 　論文類(lèi)型：期刊論文

【摘要】：目的:研究苗藥黑骨藤中咖啡�；鼘幩犷�(lèi)部位(CADF)對(duì)腫瘤壞死因子α(TNF-α)誘導(dǎo)的人類(lèi)風(fēng)濕性關(guān)節(jié)炎(RA)成纖維樣滑膜細(xì)胞MH7A增殖及炎癥因子分泌的影響,探討CADF抗RA的作用機(jī)制。方法:將MH7A細(xì)胞分為空白組、TNF-α模型組、甲氨蝶呤組(陽(yáng)性對(duì)照,20 mg/L)和CADF不同質(zhì)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(xì)胞。以TNF-α與相應(yīng)藥物的混合液共同作用24 h后,檢測(cè)細(xì)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(xì)胞介素1β(IL-1β)、白細(xì)胞介素6(IL-6)的含量。結(jié)果:與空白組比較,TNF-α模型組細(xì)胞增殖活性顯著增強(qiáng)(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(xì)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(guān)系。結(jié)論:CADF可通過(guò)抑制TNF-α誘導(dǎo)的MH7A細(xì)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(xué)民族藥與中藥開(kāi)發(fā)應(yīng)用教育部工程研究中心/國(guó)家苗藥工程技術(shù)研究中心;貴州醫(yī)科大學(xué)藥學(xué)院;貴州醫(yī)科大學(xué)貴州省藥物制劑重點(diǎn)實(shí)驗(yàn)室;
【基金】：國(guó)家自然科學(xué)基金資助項(xiàng)目(No.81460641,81660691) 貴州省優(yōu)秀青年科技人才培養(yǎng)對(duì)象專(zhuān)項(xiàng)資金項(xiàng)目(No.黔科合人字[2015]11號(hào)) 貴州省科技計(jì)劃項(xiàng)目(No.黔科合平臺(tái)人才[2016]5677 黔科合平臺(tái)人才[2016]5613) 貴州省協(xié)同創(chuàng)新中心建設(shè)項(xiàng)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(jì)劃項(xiàng)目(No.ZYRC2014012)
【分類(lèi)號(hào)】：R29
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本文編號(hào)：1554277