Effect of Sodium tanshinone II A sulfonate on Cardiomyocytes Hypertrophy Induced By Angiotensin II in Neonatal Rat
LI Shu-shen
Abstract
LI Shu-shen
Abstract
Objective To study the role of calcineurin (CaN)-dependent signaling pathway in cardiomyocytes hypertrophy and the effect of sodium tanshinone Ⅱ A sulfonate (STS) on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ)in the culture cardiomyocytes. Methods Myocytes i was determined using fura-2 labelled method by fluroscence microscope. Mitogen activated protein kinase (MAPK) and protein kinase C(PKC) and CaN activities was measured. Protein synthesis rate was measured by |Leucine incorporation as the index of cardiomyocyte hypertrophy. ResultsSynthesis rate of protein and intracellular Ca 2+ level stimulated by Ang Ⅱ in the cardiomyocytes was increased significantly (P0.01) ; STS effectively decrease the increased intracellular Ca 2+ level induced by Ang Ⅱ(P0.01 vs Ang Ⅱ group)and markedly inhibited the syntheses of protein ( P0.01 vs Ang Ⅱgroup). STS and verapamil(Ver) also suppressed the activities of the cardiomyocytes CaN and PKC stimulated by Ang Ⅱ in the cardiomyocytes. ConclusionSTS effectively decrease the increased intracellular Ca 2+ level induced by Ang Ⅱ and inhibite the activities of the CaN and PKC in cardiomyocytes.
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Objective To study the role of calcineurin (CaN)-dependent signaling pathway in cardiomyocytes hypertrophy and the effect of sodium tanshinone Ⅱ A sulfonate (STS) on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ)in the culture cardiomyocytes. Methods Myocytes i was determined using fura-2 labelled method by fluroscence microscope. Mitogen activated protein kinase (MAPK) and protein kinase C(PKC) and CaN activities was measured. Protein synthesis rate was measured by |Leucine incorporation as the index of cardiomyocyte hypertrophy. ResultsSynthesis rate of protein and intracellular Ca 2+ level stimulated by Ang Ⅱ in the cardiomyocytes was increased significantly (P0.01) ; STS effectively decrease the increased intracellular Ca 2+ level induced by Ang Ⅱ(P0.01 vs Ang Ⅱ group)and markedly inhibited the syntheses of protein ( P0.01 vs Ang Ⅱgroup). STS and verapamil(Ver) also suppressed the activities of the cardiomyocytes CaN and PKC stimulated by Ang Ⅱ in the cardiomyocytes. ConclusionSTS effectively decrease the increased intracellular Ca 2+ level induced by Ang Ⅱ and inhibite the activities of the CaN and PKC in cardiomyocytes.
Key concepts: Protein kinase C, Internal medicine, Angiotensin II, Intracellular, Chemistry, Endocrinology, Renin–angiotensin system, Myocyte