2007•Chinese Journal of HypertensionRequires access

Effect of Sodium Tanshinone II A Sulfonate on Activation of Extracellular Signal-Regulated Kinase1/2 in Angiotensin II Induced Cardiomyocyte Hypertrophy

Qiansheng Liang

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Abstract

Objective To observe effects of sodium tanshinone ⅡA sulfonate(STS) on angiotensin Ⅱ(Ang Ⅱ) induced cardiomyocyte hypertrophy and the expression of phosphorylated extracellular signal-regulated kinase1/2(p-ERK1/2).Methods Total protein in the primary culture of neonatal rat cardiomyocytes was determined by Coomassie brilliant blue and protein synthesis rate was measured by [3H]-Leucine incorporation.The expression of p-ERK1/2 was assessed using Western blot and fluorescence microscope.Results 1) The total protein and protein synthesis stimulated by Ang Ⅱ(1 μmol/L) in the cardiomyocytes were increased significantly,which was effectively attenuated by STS.2) Ang Ⅱ(1 μmol/L) promoted activation of ERK1/2 which was appeared in nucleus soon after the treatment.The translocation process of ERK1/2 induced by Ang Ⅱ was blocked by STS apparently.3)Pretreatment of cardiomyocyte with Ang Ⅱ(1 μmol/L)for 5 min,the p-ERK1/2 protein expression began to increase reaching peak effect at 10 min.STS(2,10,50 μmol/L) inhibited Ang Ⅱ induced increase in p-ERK1/2 in a dose dependent manner.Conclusion The results suggest STS significantly and dose dependently attenuated the ERK1/2 expression in the development of myocardial hypertrophy induced by Ang Ⅱ.ERK1/2 may play an important role in cardiomyocytes hypertrophy induced by Ang Ⅱ.The antihypertrophic effect of Sodium tanshinone on cardiomyocyte hypertrophy induced by Ang Ⅱ may be associated to it's effect of inhibition to ERK signaling pathway.

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Objective To observe effects of sodium tanshinone ⅡA sulfonate(STS) on angiotensin Ⅱ(Ang Ⅱ) induced cardiomyocyte hypertrophy and the expression of phosphorylated extracellular signal-regulated kinase1/2(p-ERK1/2).Methods Total protein in the primary culture of neonatal rat cardiomyocytes was determined by Coomassie brilliant blue and protein synthesis rate was measured by [3H]-Leucine incorporation.The expression of p-ERK1/2 was assessed using Western blot and fluorescence microscope.Results 1) The total protein and protein synthesis stimulated by Ang Ⅱ(1 μmol/L) in the cardiomyocytes were increased significantly,which was effectively attenuated by STS.2) Ang Ⅱ(1 μmol/L) promoted activation of ERK1/2 which was appeared in nucleus soon after the treatment.The translocation process of ERK1/2 induced by Ang Ⅱ was blocked by STS apparently.3)Pretreatment of cardiomyocyte with Ang Ⅱ(1 μmol/L)for 5 min,the p-ERK1/2 protein expression began to increase reaching peak effect at 10 min.STS(2,10,50 μmol/L) inhibited Ang Ⅱ induced increase in p-ERK1/2 in a dose dependent manner.Conclusion The results suggest STS significantly and dose dependently attenuated the ERK1/2 expression in the development of myocardial hypertrophy induced by Ang Ⅱ.ERK1/2 may play an important role in cardiomyocytes hypertrophy induced by Ang Ⅱ.The antihypertrophic effect of Sodium tanshinone on cardiomyocyte hypertrophy induced by Ang Ⅱ may be associated to it's effect of inhibition to ERK signaling pathway.

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Available abstract

Objective To observe effects of sodium tanshinone ⅡA sulfonate(STS) on angiotensin Ⅱ(Ang Ⅱ) induced cardiomyocyte hypertrophy and the expression of phosphorylated extracellular signal-regulated kinase1/2(p-ERK1/2).Methods Total protein in the primary culture of neonatal rat cardiomyocytes was determined by Coomassie brilliant blue and protein synthesis rate was measured by [3H]-Leucine incorporation.The expression of p-ERK1/2 was assessed using Western blot and fluorescence microscope.Results 1) The total protein and protein synthesis stimulated by Ang Ⅱ(1 μmol/L) in the cardiomyocytes were increased significantly,which was effectively attenuated by STS.2) Ang Ⅱ(1 μmol/L) promoted activation of ERK1/2 which was appeared in nucleus soon after the treatment.The translocation process of ERK1/2 induced by Ang Ⅱ was blocked by STS apparently.3)Pretreatment of cardiomyocyte with Ang Ⅱ(1 μmol/L)for 5 min,the p-ERK1/2 protein expression began to increase reaching peak effect at 10 min.STS(2,10,50 μmol/L) inhibited Ang Ⅱ induced increase in p-ERK1/2 in a dose dependent manner.Conclusion The results suggest STS significantly and dose dependently attenuated the ERK1/2 expression in the development of myocardial hypertrophy induced by Ang Ⅱ.ERK1/2 may play an important role in cardiomyocytes hypertrophy induced by Ang Ⅱ.The antihypertrophic effect of Sodium tanshinone on cardiomyocyte hypertrophy induced by Ang Ⅱ may be associated to it's effect of inhibition to ERK signaling pathway.

Key concepts: Angiotensin II, Extracellular, Western blot, MAPK/ERK pathway, Internal medicine, Endocrinology, Renin–angiotensin system, Muscle hypertrophy

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Effect of Sodium Tanshinone II A Sulfonate on Activation of Extracellular Signal-Regulated Kinase1/2 in Angiotensin II Induced Cardiomyocyte Hypertrophy — Research Paper | ScholarLens