Effect of sodium tanshinone II A sulfonate on cardiac myocyte hypertrophy and its underlying mechanism.
- Author:
Jun FENG
1
,
2
;
Zhi ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Animals, Newborn; Cell Survival; drug effects; Gene Expression Regulation; drug effects; Hypertrophy; Leucine; metabolism; Myocytes, Cardiac; drug effects; pathology; Phenanthrenes; pharmacology; Proto-Oncogene Proteins c-fos; genetics; metabolism; RNA, Messenger; genetics; metabolism; Rats; Rats, Wistar; Time Factors; Tritium
- From: Chinese journal of integrative medicine 2008;14(3):197-201
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo 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.
METHODSThe 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).
RESULTSSTS 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.
CONCLUSIONSTS 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.
