摘要
目的通过观察PKA拮抗剂H-89和CRF受体拮抗剂Astressin抑制UCN诱导乳大鼠心肌细胞肥厚的作用,研究UCN诱导的大鼠心肌细胞肥厚的信号转导机制。方法以体外培养的乳大鼠心肌细胞为模型,应用UCN 0.1μmol.L-1诱导心肌肥大,观察H-89 0.1μmol.L-1和Astressin 1μmol.L-1的作用,探讨UCN 0.1μmol.L-1对心肌肥厚的作用机制。用消化分离法及计算机图像分析系统检测心肌细胞体积;[3H]亮氨酸掺入法测定心肌细胞蛋白的合成;用Western蛋白印迹法测定ANP表达。结果UCN0.1μmol.L-1使心肌细胞体积、蛋白合成和ANP表达明显增加,H-89 0.1μmol.L-1和Astressin 1μmol.L-1抑制UCN诱导的心肌肥大。结论Urocortin可能通过CRF-R2并通过PKA信号通路诱导乳大鼠心肌细胞肥大。
Objective To observe the inhibitive effects and signal transduction by H -89 and CRF receptor antagonist Astressin on hypertrophic myocardial cells induced by UCN in neonatal rats and study the signal transduction mechanism of hypertrophic myocar- dial rats induced by UCN. Methods Using the myocardial cells of neonatal rats cultured in vitro as models, and inducing myocardial hypertrophy by using UCN 0. 1 μmol·L^-1 to observe the effect of H -89 0. 1μmol·L^-1and Astressin 1μmol·L^-1 and discuss the mechanism of effect of UCN 0. 1μmol·L^-1 on myocardial hypertrophy. The cardiomyocytes volumes were measured by computer pho- togTaph analysis system. The protein synthetic rate was obtained through measuring the incorporation of [ 3H ] -leucine into myocyte protein by liquid scintillation method. The expression of ANP was deternained by western - blot. Results UCN enhanced the cardiomyocyte volume, the synthesis and the expression of ANP. H - 89 0. 1μmol·L^-1 and Astressin 1 μmol·L^-1 can inhibit myocardial cells hypertrophy induced by UCN. Conclusions The hypertrophic effect of UCN in neonatal rats cardiomyocytes is mediated via CRF - R2. and activation of the PKA pathway.
出处
《辽宁医学院学报》
CAS
2009年第2期119-121,151,共4页
Journal of Liaoning Medical University (LNMU) Bimonthly
基金
辽宁省自然科学基金资助项目
编号:20042170
