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目的主要从丝裂原活化蛋白激酶(MAPK)激活及失活的角度研究丹参酮ⅡA磺酸钠(STS)对血管紧张肽Ⅱ(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]-亮氨酸掺入法测定蛋白合成速率作为心肌肥大指标；用Western blot测定磷酸化MAPK蛋白(p44MAPK、p42MAPK)表达。结果①AngⅡ(1μmoL/L)处理24h,心肌细胞[~3H]-亮氨酸掺入率、蛋白含量明显增加,STS能明显抑制AngⅡ介导心肌细胞[~3H]-亮氨酸掺入率、蛋白含量的增加。②用AngⅡ(1μmol/L)处理心肌细胞5min,磷酸化MAPK蛋白(p44MAPK、p42MAPK)表达即开始增加,10min左右时最明显。以AngⅡ(1μmol/L)处理心肌细胞10min,磷酸化MAPK蛋白(p44MAPK、p42MAPK)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MAPK蛋白表达。③预先以不同浓度STS处理心肌细胞30 min,发现STS对AngⅡ诱导的心肌细胞磷酸化MAPK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MAPK表达有关。
Objective To study the effect of sodium tanshinone IIA sulfonate (STS) on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy from the perspective of activation and inactivation of mitogen-activated protein kinase (MAPK). Methods Neonatal rat cardiomyocytes were cultured, protein content of cardiomyocytes was measured by Coomassie brilliant blue method, protein synthesis rate was measured by [~3H]-leucine incorporation method as an index of cardiac hypertrophy, and phosphorylated MAPK protein (p44MAPK, p42MAPK) was determined by Western blot. )expression. Results AngII (1μmol/L) treatment for 24h, myocardial cell [~3H]-leucine incorporation rate, protein content increased significantly, STS can significantly inhibit AngII-mediated [~ 3H]-leucine incorporation rate of myocardial cells, Increase in protein content. 2 After treated with AngII (1μmol/L) for 5min, the expression of phosphorylated MAPK protein (p44MAPK, p42MAPK) began to increase, and it was the most obvious at around 10min. Cardiomyocytes were treated with Ang II (1 μmol/L) for 10 min. The expression of phosphorylated MAPK protein (p44MAPK, p42MAPK) was the standard. Cardiomyocytes were treated with STS (2, 10, and 50 μmol/L) for 30 min. STS was found to significantly inhibit Ang II induction. Cardiomyocytes Phosphorylated MAPK Protein Expression. 3 Pretreatment of cardiomyocytes with different concentrations of STS for 30 min revealed a dose-dependent inhibitory effect of STS on AngII-induced phosphorylation of MAPK protein in cardiomyocytes. Conclusion STS can inhibit Ang II-induced cardiac hypertrophy, and its mechanism is related to the inhibition of phosphorylated MAPK expression.