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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 paclitaxel (anticancer drug) on angiotensin Ⅱ (Ang Ⅱ) induced phenotype of rat adventitial fibroblasts (AF). Methods Male Sprague-Dawley rats were selected and adventitial artery-adventitial fibroblasts were cultured with paclitaxel (0, 10, 30, and 90 nmol.L-1) for 12 h respectively to determine the concentration of paclitaxel that did not affect the viability of AF. The AF was divided into two groups: AngⅡgroup and AngⅡ + 9nmol.L-1 paclitaxel group. The mRNA and α-SM-actin mRNA expression of α-SM-actin were detected by RT-PCR and Western blot respectively. Protein. When the concentration of paclitaxel was lower than 10nmol.L-1, the killing effect of paclitaxel on fibroblasts was weak, and there was no significant difference between paclitaxel and paclitaxel group. Low concentration paclitaxel effectively reduced Angα-induced AFα-SM-actin at mRNA and protein levels Expression (P <0.05). Conclusions Trace paclitaxel can inhibit the phenotypic transformation of AF in rats and may be one of the mechanisms of paclitaxel-induced stent restenosis.