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STS对AngⅡ诱导的心肌肥厚及p-ERK1/2、MKP-1表达的影响 被引量:3

Effects of sodium tanshinone ⅡA sulfonate on AngⅡ-induced cardiomyocyte hypertrophy and the expressions of p-ERK1/2 and MKP-1
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摘要 目的观察丹参酮ⅡA磺酸钠(STS)对血管紧张素Ⅱ(A ngⅡ)诱导的心肌肥厚及磷酸化细胞外信号调节蛋白激酶(p-ERK 1/2)、丝裂原活化蛋白激酶磷酸酶-1(M KP-1)表达的影响。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;W esternb lot法测定p-ERK 1/2、M KP-1表达。结果STS能显著降低A ngⅡ诱导的心肌细胞蛋白含量、蛋白合成速率的上升;对p-ERK 1/2表达具有剂量依赖性的抑制作用;同时上调M KP-1表达。结论STS可以抑制A ngⅡ诱导的心肌肥厚,其机制与上调M KP-1表达,降低p-ERK 1/2表达有关。 [Objective] To observe effects of sodium tanshinone ⅡA sulfonate (STS) on angiotensin Ⅱ (Ang Ⅱ)-induced cardiomyocyte hypertrophy and the expressions of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and mitogen-activated protein kinase phosphatase-1 (MKP-1). [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 expressions of p-ERK1/2 and MKP-1 were assessed by using Western blot. [Results] STS could decrease AngⅡ -induced elevations of the total protein and protein synthesis rate and inhibit the expression of p-ERK1/2 in a dose-dependent manner and upregulate the expression of MKP-1. [Conclusion] The anti-hypertrophic effect of STS on Ang Ⅱ -induced cardiomyocyte hypertrophy is associated with inhibition of ERK1/2 signaling pathway via upregulation of MKP-1.
出处 《山东医药》 CAS 北大核心 2006年第28期1-3,共3页 Shandong Medical Journal
基金 国家自然科学基金资助项目(30500657)。
关键词 丹参酮Ⅱ A磺酸钠 心肌肥厚 细胞外信号调节激酶 丝裂原活化蛋白激酶磷酸酶-1 sodium tanshinone Ⅱ A sulfonate cardiomyocyte hypertrophy extracellular signal-regulated kinase mitogen-activated protein kinase phosphatase-1
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