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作 者:沈凯[1] 杨喆娟 袁国裕[1] 顾磊科[1] 王红娜[1] 陈国雄[1] 方波[1]
出 处:《中国临床药理学杂志》2010年第8期615-618,共4页The Chinese Journal of Clinical Pharmacology
基 金:浙江省医药卫生科学研究基金资助项目(2007A198);浙江省中医药科技计划基金资助项目(2007CA129)
摘 要:目的观察紫杉醇(抗癌药)对血管紧张素Ⅱ(AngⅡ)诱导的大鼠降主动脉外膜成纤维细胞(AF)表型转化的影响。方法选取雄性SD大鼠,贴壁法培养降主动脉外膜AF,分别以0,10,30,90nmol.L-1的紫杉醇干预12h,确定对AF生存活力无影响的紫杉醇浓度。取AF分成2组:AngⅡ组及AngⅡ+9nmol.L-1紫杉醇组,分别采用RT-PCR法和Western印迹法检测α-平滑肌肌动蛋白(α-SM-actin)mRNA及α-SM-actin蛋白表达。结果低于10nmol.L-1时,紫杉醇对成纤维细胞的杀伤作用较弱,与未加紫杉醇组无明显差异;低浓度紫杉醇在mRNA水平和蛋白水平均有效降低AngII诱导的AFα-SM-actin表达(P<0.05)。结论微量紫杉醇可抑制大鼠AF的表型转化,可能为紫杉醇支架减缓血管再狭窄的机制之一。Objective To investigate the effect of taxol on the phenotype transformation of adventitial fibroblast cells (AF) induced by angiotensin Ⅱ ( Ang Ⅱ ). Methods AF were isolated from thoracic aortas of male Sprague Dawly (SD) rats. The AF were allocated into 4 groups : 0,10, 30, 90 nmol · L^- 1 taxol, to identify the lowest concentration of taxol that did not affect the survival rate of AF. Then the AF were allocated into 2 groups: Ang Ⅱ group and Ang Ⅱ + 9 nmol · L^-1 taxol group. The expression of α - smooth muscle actin ( α - SM - actin) on mRNA levels and protein levels were detected by RT - PCR and Western blotting respectively. Results The concentration of taxol that did not affect the survival rate of AF was lower than 10 nmol · L^-1. Taxol significantly inhibited the phenotype transformation of AF induced by Angiotensin Ⅱ on mRNA levels and protein levels (P 〈 0. 05 ). Conclusion Low dose of taxol could effectively inhibit the phenotype transformation of AF, therefore inhibit restenosis after coronary stenting.
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