丹参酮ⅡA磺酸钠影响AngⅡ诱导心肌细胞肥大反应及p-p38,MKP-1表达

Effects of Sodium Tanshinone ⅡA Sulfonate on Ang Ⅱ-Induced Cardiomyocyte Hypertrophy and Expressions of p-p38 and MKP-1

目的观察丹参酮ⅡA磺酸钠(Sodium tanshinoneⅡA sulfonate,STS)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌细胞肥大反应及p-p38,MKP-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细胞肥大指标;用Western-blot测定p-p38,MKP-1表达。结果STS能显著降低AngⅡ诱导的心肌细胞蛋白含量、蛋白合成速率上升;对p-p38表达具有显著抑制作用;同时上调MKP-1表达。结论STS可以抑制AngⅡ诱导的心肌细胞肥大反应,机制与上调MKP-1表达,降低p-p38表达有关。

OBJECTIVE To observe effects of Sodium tanshinone ⅡA sulfonate （STS） on angiotensin Ⅱ （Ang Ⅱ）-induced cardiomyoeyte hypertrophy and expressions of phosphorylated p38 （p-p38） and mitogen-aetivated 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 eoomassie brilliant blue and protein synthesis rate was measured by [ ^3H ]-Leueine incorporation. The expressions of p-p38 and MKP-1 were assessed using Western blotting. RESULTS STS decreased Ang H-induced elevations of the total protein and protein synthesis rate ,inhibited the expression of p-p38 and upregulated the expression of MKP-1. CONCLUSION The anti-hypertrophic effects of STS on Ang H-induced cardiomyocyte hypertrophy were associated with the inhibition of p38 signal pathway via upregulation of MKP-1.