中文摘要：

目的 从细胞外信号调节激酶1／2（ERK1／2）激活角度研究丹参酮ⅡA磺酸钠（sodium tanshinone Ⅱ A sulfonate，STS）对血管紧张素Ⅱ（angiotensinⅡ，AngⅡ）诱导的心肌肥大反应中的作用。方法 培养新生大鼠心肌细胞，考马斯亮蓝法测定心肌细胞蛋白含量、[^3H]-亮氨酸参人法测定蛋白合成速率作为心肌肥大指标；用免疫荧光标记法和Western blot测定磷酸化ERK1／2蛋白（p-ERK1／2）表达。结果 （1）AngⅡ（1μmol·L^-1）处理24h，心肌细胞[^3H]-亮氨酸参人率、蛋白含量明显增加，STS能明显抑制AngⅡ介导心肌细胞[^3H]-亮氨酸参人率、蛋白含量的增加；（2）AngⅡ刺激心肌细胞可见胞核内出现磷酸化ERK1／2荧光染色，丹参酮ⅡA可阻断AngⅡ引起的ERK1／2活化、人核过程；（3）用AngⅡ（μmol·L。）处理心肌细胞5min，磷酸化ERK1／2蛋白（p-ERK1／2）表达即开始增加，10min左右时最明显。以AngⅡ（1μmol·L^-1）处理心肌细胞10min，磷酸化ERK1／2蛋白（p-ERK1／2）表达为标准，预先以STS（2，10，50μmol·L。）处理心肌细胞30min，发现STS可明显抑制AngⅡ诱导的心肌细胞磷酸化ERK1／2蛋白表达；（4）预先以不同浓度STS处理心肌细胞30min，发现STS对AngⅡ诱导的心肌细胞磷酸化ERK1／2蛋白表达的抑制作用存在剂量依赖性。结论STS可以抑制AngⅡ诱导的心肌肥厚，其机制与抑制磷酸化ERK1／2表达有关。

英文摘要：

Aim To observe effects of Sodium tanshi- none Ⅱ A sulfonate （STS） on angiotension Ⅱ （ Ang Ⅱ ） - induced cardiomyocyte hypertrophy and the expression of phosphorylated extracellular signal-regulated kinase1/2 （p-ERK1/2）. Methods In the primary culture of neonatal rat cardiomyocytes, as indexes of cardiomyocyte hypertrophy, the total protein was determined by coomassie brilliant blue and protein synthesis rate was measured by [^3H ]-Leucine incorporation. The expression of p-ERK1/2 was assessed using Western blot and fluorescence microscope. Results ① The total protein and protein synthesis rate stimulated by Ang Ⅱ （ 1 μmol· L^-1 ） in the cardiomyocytes increased significantly in contrast to that of control; STS could effectively decrease the increased total protein level induced by Ang Ⅱ and markedly inhibit synthesis of protein. ② Ang Ⅱ （ 1μmol · L^-1 ） had the effect of promoting activation of ERK1/2 and then appeared in nucleus rapidly. The translocation process of ERK1/2 induced by Ang Ⅱ was blocked distinctly by STS. ③ Cardiomyocyte pretreated with Ang Ⅱ （ 1μmol · L^-1 ） for 5 min, the p-ERK1/2 protein expression began to increase , the peak effect was at 10 min. While pretreatment with STS（2, 10, 50μmol · L^-1） ,Ang Ⅱ- induced increase in p-ERK1/2 were inhibited evidently. ③In pretreatment of cardiomyocyte with STS in different doses for 30 min, STS was found to be able to inhibit the expression of p-ERK1/2 stimulated by Ang Ⅱ in a dose-dependent manner. Conclusions The results suggested that activation of ERK1/2 might play an important role in cardiomyocytes hypertrophy induced by Ang Ⅱ , and the anti-hypertrophic effect of STS on cardiomyocyte hypertrophy induced by Ang Ⅱ might be associated to its inhibitory effect on ERK signaling pathway.