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作 者:王雨娟[1] 郑家润[1] 李新宇[1] 张志文[2]
机构地区:[1]中国医学科学院,中国协和医科大学皮肤病研究所,江苏南京210042 [2]北京大学生理系,北京100083
出 处:《临床皮肤科杂志》2003年第6期329-331,共3页Journal of Clinical Dermatology
摘 要:目的:探索沙利度胺、氨苯砜、雷公藤内酯醇等药物对内皮细胞诱导性细胞间黏附分子-1(ICAM-1)表达的影响。方法:用逆转录-聚合酶链反应(RT-PCR)方法检测肿瘤坏死因子-α(TNF-α)、佛波酯(PMA)或脂多糖(LPS)对人内皮细胞株ECV304细胞上ICAM-1表达的诱导,以及沙利度胺、氨苯砜、雷公藤内酯醇、吲哚美辛、丙酸氯倍他索等药物对ECV304细胞上诱导性ICAM-1表达的影响。结果:TNF-α和PMA可显著上调ECV304细胞上ICAM-1的表达;沙利度胺、氨苯砜可分别抑制TNF-α或PMA诱导的ICAM-1表达;吲哚美辛可显著上调ECV304细胞上ICAM-1的诱导表达。结论:沙利度胺和氨苯砜的抗炎作用可能与其对内皮细胞上ICAM-1表达的抑制有关。Objective:To investigate the effect of thalidomide,dapsone and triptolide on the expression of intercellular ad-hesion molecule-1(ICAM-1)in endothelial cells.Methods:The induced ICAM-1expressions by tumor necrosis factor(TNF)-α,phorbol12-myristate13-acetate(PMA)or lipopolysaccharide(LPS)were detected by RT-PCR in human endothelial cell lines(ECV304).Furthermore the effects of thalidomide,dapsone,triptolide,clobetasol propionate and indomethacin on this ex-pression of ICAM-1were detected by RT-PCR as well.Results:The expression of ICAM-1were markedly upregulated by the stimulation of TNF-αor PMA.Thalidomide potently suppressed TNF-α-induced ICAM-1expression in ECV304cells.Dapsone also significantly suppressed PMA-induced ICAM-1expression.In contrast,indomethacin increased the ICAM-1ex-pression which induced by both TNF-αand PMA.Conclusion:The inhibitory effects of thalidomide and dapsone on in-ducible expression of ICAM-1in endothelial cells represent a molecular mechanism that contributes to the anti-inflammatory property of these drugs.
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