Extract of Ginkgo biloba and quercetin inhibit angiotensin-II induced hypertrophy in cultured neonatal rat cardiomyocytes.
- Author:
Yang WU
1
;
Yu-mei GU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Cells, Cultured; Drugs, Chinese Herbal; pharmacology; Extracellular Signal-Regulated MAP Kinases; metabolism; Ginkgo biloba; JNK Mitogen-Activated Protein Kinases; metabolism; Myocytes, Cardiac; drug effects; metabolism; pathology; Plant Extracts; pharmacology; Quercetin; pharmacology; Rats; Rats, Sprague-Dawley; Signal Transduction
- From: Chinese Journal of Cardiology 2006;34(5):454-457
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect and related mechanisms of extract of ginkgo biloba (EGb) and quercetin (Que) on angiotensin II (AngII) induced hypertrophy in the primary cultured neonatal rat cardiomyocytes.
METHODSPrimary cultured neonatal rat cardiomyocytes were treated with placebo (control), AngII (10(-6) mol/L), AngII + EGb (40 microg/ml), AngII + Que (4 microg/ml), AngII + captopril (10(-5) mol/L) and AngII + DPI [diphenylene iodonium chloride, NADPH inhibitor (10 micromol/L)] respectively. Total protein content of cardiomyocytes, cardiomyocytes size, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. The expression of phospho-Extracellular-signal regulated kinase 1/2, phospho-c-Jun N-terminal kinase and phospho-P38 were detected by Western blot.
RESULTSThe total protein content and cell size of cardiomyocytes increased significantly in AngII treated cells and these effects could be blocked by EGb and Que. EGb and Que also enhanced the SOD activity and reduced the production of MDA. AngII significantly activated ERK1/2, JNK and P38 expressions and only JNK activation could be inhibited by Que and DPI.
CONCLUSIONEGb and Que can inhibit AngII-induced cardiomyocyte hypertrophy through a ROS-dependent pathway. Que could also block the JNK activation induced by AngII.
