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目的观察尾加压素Ⅱ(Urotensin Ⅱ,U Ⅱ)对心肌细胞肥大的效应。方法以体外培养的SD乳鼠心肌细胞为实验模型,分为正常对照组,单纯UⅡ作用组,环胞素A(CsA)阻断组。用real-time PCR方法分析β-MHC、CaN(钙调神经磷酸酶) mRNA表达的变化,用免疫印迹法(Western blot)研究心肌肥大过程中β-MHC、CaN蛋白表达的变化,探讨UⅡ对心肌细胞肥大的影响。结果①随着UⅡ浓度的增加,心肌细胞β-MHC、CaN mRNA和蛋白表达明显增加,其中10-8、10-7mol/L U Ⅱ组与对照组相比较差异显著(P<0.05);②用10-8mol/L U Ⅱ处理心肌细胞12、24、48 h,随着时间增加,心肌细胞β-MHC、CaN mRNA和蛋白表达呈递增趋势,其中处理24h组与正常对照组有显著差异(P<0.05);③预先用环胞素A5μmol/L(cyclosporin A CsA)处理正常心肌细胞24 h,然后用10-8mol/L U Ⅱ作用24 h,心肌细胞β-MHC、CaN mRNA和蛋白表达与正常心肌细胞经10-8mol/L U Ⅱ单纯作用24 h差异有显著意义(P<0.05)。结论 U Ⅱ能够诱导心肌细胞的肥大,环胞素A(CsA)能阻断此效应,CaN参与了UⅡ诱导的心肌肥大过程。
Objective To observe the effect of urotensin Ⅱ (U Ⅱ) on cardiomyocyte hypertrophy. Methods The cultured neonatal rat cardiomyocytes were divided into normal control group, UⅡ-treated group and CsA-blocking group. The changes of β-MHC and CaN (calcineurin) mRNA expression were analyzed by real-time PCR. The changes of β-MHC and CaN protein expression in myocardial hypertrophy were detected by Western blotting, Effects of hypertrophy on cardiomyocytes. Results ① The expressions of β-MHC, CaN mRNA and protein in cardiomyocytes were significantly increased with the increase of UⅡ concentration, and the difference was significant (P <0.05) between 10-8,10-7mol / LU Ⅱ group and control group; The cardiomyocytes were treated with 10-8mol / LU Ⅱ for 12, 24 and 48 h. The expression of β-MHC and CaN mRNA and protein in cardiomyocytes increased with the increase of time, and there was a significant difference between the 24h group and the normal control group (P < 0.05). ③ The normal cardiomyocytes were treated with cyclosporin A CsA for 24 h and then treated with 10-8 mol / LU Ⅱ for 24 h. The expressions of β-MHC, CaN mRNA and protein in cardiomyocytes were similar to those in normal myocardium The difference of cells treated with 10-8mol / LU Ⅱ for 24 h was significant (P <0.05). Conclusion U Ⅱ can induce the hypertrophy of cardiomyocytes. CsA can block this effect, and CaN participates in U Ⅱ induced hypertrophy.