摘要
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 explore the mechanism by which urotensin Ⅱ induces hypertrophy of the cultured rat cardiomyocytes. Methods The cultured cardiomyocytes from neonatal SD rats were treated with urotensin Ⅱ , also with cyclosporine A for its blocking effect on urotensin Ⅱ induced cardiomyocytes hypertrophy. The mRNA and protein levels of ^-MHC and CaN were evaluated by real-time PCR and Western blotting, respectively. Results In the cells treated with 10^-8 and 10^-7mol/L urotensin Ⅱ, the mRNA and protein levels of β-MHC and CaN were significantly higher than that of control （P 〈 0.05 ）. Treatment of cardiomyocytes with 10^-8 mol/L urotensin Ⅱ for 12 -48 h induced a time-dependent increase of β-MHC and CaN mRNA and protein expressions （P 〈 0.05）. Urotensin Ⅱ -induced upregulation of β-MHC and CaN mRNA and protein expressions can be abated by 24-hour cyclosporine A pretreatment （P 〈0.05）. Conclusion Urotensin Ⅱ can induce cardiomyocytes hypertrophy and eyclosporine A can block this effect. CaN participates in this process. Our results may contribute to the investigation of cardiaomyocyts hypertrophy induced by hypertension and other cardiac diseases.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2008年第24期2293-2295,共3页
Journal of Third Military Medical University
基金
重庆市自然科学基金(2007BB5026)~~
