Effect of Sodium Tanshinone II A Sulfonate on Activation of Extracellular Signal-Regulated Kinase1/2 in Angiotensin II Induced Cardiomyocyte Hypertrophy
Qiansheng Liang
Abstract
Qiansheng Liang
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.
Key concepts: Angiotensin II, Extracellular, Western blot, MAPK/ERK pathway, Internal medicine, Endocrinology, Renin–angiotensin system, Muscle hypertrophy