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Effect of sodium tanshinone II A sulfonate on cardiac myocyte hypertrophy and its underlying mechanism
  
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KeyWord:sodium tanshinone II A sulfonate  angiotensin II  cardiac myocyte hypertrophy  c-fos
Author NameAffiliationE-mail
Jun Feng Department of Emergency Internal Medicine, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China andyterry555@163.com 
Zhi Zheng Department of Emergency Internal Medicine, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, 430030, China  
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Abstract:
      OBJECTIVE: To investigate the effects of sodium tanshinone II A sulfonate (STS) on the hypertrophy induced by angiotensin II (Ang II) in primary cultured neonatal rat cardiac myocytes. METHODS: The effect of STS on cytotoxicity was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-3,5-phenytetrazoliumromide (MTT) assay. As indexes for cardiocyte hypertrophy, cell size was determined by phase contrast microscopy and protein synthesis rate was measured by 3H-leucine incorporation. The proto-oncogene c-fos mRNA expression of cardiocytes was assessed using reverse transcription polymerase chain reaction (RT-PCR). RESULTS: STS could inhibit cardiocyte hypertrophy, increase the protein synthesis rate and enhance proto-oncogene c-fos mRNA expression in cardiocytes induced by Ang II (P<0.01), with an effect similar to that of Valsartan, the Ang II receptor antagonist. CONCLUSION: STS can prevent the hypertrophy of cardiac myocytes induced by Ang II, which may be related to its inhibition of the expression of proto-oncogene c-fos mRNA.
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