Effects of tetrandrine on Ang II-induced cardiomyocyte hypertrophy and p-ERK1/2 expression.
- Author:
Dai-Xing ZHOU
1
;
Guang-Tian YANG
;
Xue-Xin HE
;
Qiang LIU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; toxicity; Animals; Animals, Newborn; Benzylisoquinolines; isolation & purification; pharmacology; Blotting, Western; Cell Size; drug effects; Cells, Cultured; Drugs, Chinese Herbal; isolation & purification; pharmacology; Hypertrophy; Immunoprecipitation; Microscopy, Phase-Contrast; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Myocytes, Cardiac; drug effects; metabolism; pathology; Phosphorylation; drug effects; Plants, Medicinal; chemistry; Protein Biosynthesis; drug effects; Rats; Rats, Sprague-Dawley; Signal Transduction; Stephania tetrandra; chemistry
- From: China Journal of Chinese Materia Medica 2007;32(18):1921-1924
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe effects of tetrandrine (Tet) on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy and the activity and expression of phosphorylated ERK1/2 (p-ERK1/2).
METHODIn the primary culture of neonatal rat cardiomyocytes, as indexes of cardiomyocyte hypertrophy, pulsation rate was measured under phase contrast microscope. Cell size was determined by cell morphology analytical system. The total protein was determined by coomassie brilliant blue and protein synthesis rate was measured by [3H]-Leucine incorporation. ERK activity was measured by immuno-precipitation. The expression of p-ERK1/2 was assessed using Western blot.
RESULTTet can decrease Ang II-induced elevations of the pulsation rate, cell size, total protein and protein synthesis rate; inhibit the activity and expression of p-ERK1/2.
CONCLUSIONThe anti-hypertrophic effect of Tet on Ang II-induced cardiomyocyte hypertrophy was associated with inhibition of ERK1/2 signaling pathway.
