2006•Chinese Journal of Critical Care MedicineRequires access

Effect of Sodium tanshinone IIA sulfonate on cardiomyocytes hypertrophy of neonatal rat

Zhi Ping Zheng

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Abstract

Objectives To study the role of calcineurin(CaN)-dependent signaling pathway in cardiomyocytes hypertrophy by observing the affection of Sodium tanshinone ⅡA sulfonate(STS) on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ)in the primary culture of neonatal rat cardiomyocytes.Methods Upon the model of the primary culture of neonatal rat cardiomyocytes,Ca~(2+) releasing from Ca~(2+) stores stimulated by Ang Ⅱ,interfering with verapamil(Ver) and STS;detecting intracellular Ca~(2+) level and the activities of the cardiomyocytes CaN;protein synthesis rate was measured by -Leucine incorporation as the index of cardiomyocyte hypertrophy.CaN expression of protein was assessed using Western blot.The proto-oncogene c-fos mRNA expression was assessed with reverse transcription polymerase chain reaction(RT-PCR).Results Synthesis rate of protein and intracellular Ca~(2+) level stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.01);STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱ(P0.01 vs Ang Ⅱgroup)and markedly inhibited syntheses of protein(P0.01 vs Ang Ⅱ group).The activities and protein expression of the cardiomyocytes CaN and the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.05,P0.01,P0.01).STS and Ver also suppressed the activities and protein expression of the cardiomyocytes CaN the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes.Conclusion The study indicates CaN signaling pathway is important in cardiomyocytes hypertrophy induced by Ang Ⅱ;STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱto inhibite the activities and protein expression of the cardiomyocytes CaN to decreased the expression of proto-oncogene c-fos mRNA for cardiomyocytes hypertrophy.

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Objectives To study the role of calcineurin(CaN)-dependent signaling pathway in cardiomyocytes hypertrophy by observing the affection of Sodium tanshinone ⅡA sulfonate(STS) on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ)in the primary culture of neonatal rat cardiomyocytes.Methods Upon the model of the primary culture of neonatal rat cardiomyocytes,Ca~(2+) releasing from Ca~(2+) stores stimulated by Ang Ⅱ,interfering with verapamil(Ver) and STS;detecting intracellular Ca~(2+) level and the activities of the cardiomyocytes CaN;protein synthesis rate was measured by -Leucine incorporation as the index of cardiomyocyte hypertrophy.CaN expression of protein was assessed using Western blot.The proto-oncogene c-fos mRNA expression was assessed with reverse transcription polymerase chain reaction(RT-PCR).Results Synthesis rate of protein and intracellular Ca~(2+) level stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.01);STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱ(P0.01 vs Ang Ⅱgroup)and markedly inhibited syntheses of protein(P0.01 vs Ang Ⅱ group).The activities and protein expression of the cardiomyocytes CaN and the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.05,P0.01,P0.01).STS and Ver also suppressed the activities and protein expression of the cardiomyocytes CaN the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes.Conclusion The study indicates CaN signaling pathway is important in cardiomyocytes hypertrophy induced by Ang Ⅱ;STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱto inhibite the activities and protein expression of the cardiomyocytes CaN to decreased the expression of proto-oncogene c-fos mRNA for cardiomyocytes hypertrophy.

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Available abstract

Objectives To study the role of calcineurin(CaN)-dependent signaling pathway in cardiomyocytes hypertrophy by observing the affection of Sodium tanshinone ⅡA sulfonate(STS) on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ)in the primary culture of neonatal rat cardiomyocytes.Methods Upon the model of the primary culture of neonatal rat cardiomyocytes,Ca~(2+) releasing from Ca~(2+) stores stimulated by Ang Ⅱ,interfering with verapamil(Ver) and STS;detecting intracellular Ca~(2+) level and the activities of the cardiomyocytes CaN;protein synthesis rate was measured by -Leucine incorporation as the index of cardiomyocyte hypertrophy.CaN expression of protein was assessed using Western blot.The proto-oncogene c-fos mRNA expression was assessed with reverse transcription polymerase chain reaction(RT-PCR).Results Synthesis rate of protein and intracellular Ca~(2+) level stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.01);STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱ(P0.01 vs Ang Ⅱgroup)and markedly inhibited syntheses of protein(P0.01 vs Ang Ⅱ group).The activities and protein expression of the cardiomyocytes CaN and the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes increased significantly in contrast to control(P0.05,P0.01,P0.01).STS and Ver also suppressed the activities and protein expression of the cardiomyocytes CaN the c-fos mRNA expression stimulated by Ang Ⅱin the cardiomyocytes.Conclusion The study indicates CaN signaling pathway is important in cardiomyocytes hypertrophy induced by Ang Ⅱ;STS can effectively decrease the increased intracellular Ca~(2+) level induced by Ang Ⅱto inhibite the activities and protein expression of the cardiomyocytes CaN to decreased the expression of proto-oncogene c-fos mRNA for cardiomyocytes hypertrophy.

Key concepts: Intracellular, Internal medicine, Messenger RNA, Endocrinology, Muscle hypertrophy, Western blot, Angiotensin II, Myocyte

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