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作 者:黄建林[1] 吴玉琼[1] 罗敏琪[1] 魏秋静[1] 余步云[1] 古洁若[1]
机构地区:[1]中山大学附属第三医院风湿免疫科,广州510630
出 处:《中华风湿病学杂志》2008年第9期613-615,共3页Chinese Journal of Rheumatology
基 金:基金项目:广东省自然科学基金资助项目(5001793)
摘 要:目的进一步研究青藤碱(SIN)对肿瘤坏死因子(TNF)-α诱导脐静脉内皮细胞(HUVECs)血管细胞黏附分子(VCAM)-1表达的影响。方法从新鲜脐带中分离培养HUVECs。用TNF-α诱导HUVECs表达VCAM-l,实验组加入不同浓度的SIN(0.25、0.5和1.0mol/L)或地塞米松(1.0×10^-6mol/L)分别进行或联合进行干预,用流式细胞仪检测细胞表面VCAM-1表达。结果与TNF-α刺激组相比,SIN干预组细胞表面VCAM-1表达下降,抑制作用以1.0mol/L最为显著。联合地塞米松(1.0×10^-6 mol/L)进行干预,可加强SIN对TNF-α诱导的VCAM-1表达的抑制作用。结论SIN可抑制TNF-α诱导的脐静脉内皮细胞VCAM-1的表达。青藤碱与地塞米松对TNF-α诱导的VCAM-1表达的抑制有协同作用。Objective To further investigate the effect of sinomenine (SIN) on TNF-α-indueed VCAM-1 expression in human umbilical vein endothelial cells (HUVECs). Methods HUVECs were isolated from freshly collected umbilical cords. Positive control samples were stimulated with TNF-α, but free of SIN. Negative control samples were treated in the same way, but without TNF-α and SIN. Experimental samples were cocuhured with TNF-α and SIN at various concentrations (0.25, 0.5, and 1.0 mol/L), or TNF-α and dexamethasone (Dex) at concentration of 1.0×l0^-6 mol/L,or TNF-α with Dex (at concentration of 1.0×l0^-6 mol/L) and SIN at different concentrations (0.25, 0.5, and 1.0 mmol/L) (co-treated groups). VCAM-1 expression was detected by flow cytometry (FCM). Results SIN inhibited expression of VCAM-1 in TNF-α-induced HUVECs, the best effect was shown in the 1.0mmol/L SIN treated group. VCAM-1 decreased more markedly in the cotreated groups. Conclusion SIN inhibits TNF-α-induced VCAM-1 expression on HUVECs in vitro, and SIN maybe synergistic with Dex in inhibiting TNF-α-induced VCAM-1 expression on HUVECs in vitro.
关 键 词:青藤碱 血管细胞黏附分子-1 人脐静脉内皮细胞
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