Effect of EGb and quercetin on culture neonatal rat cardiomyocytes hypertrophy and mechanism.
- Author:
Yang WU
1
;
Yu-mei GU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Cell Size; drug effects; Cells, Cultured; Ginkgo biloba; chemistry; MAP Kinase Signaling System; Malondialdehyde; analysis; Myocytes, Cardiac; cytology; drug effects; metabolism; Plant Extracts; pharmacology; Quercetin; pharmacology; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; metabolism
- From: Chinese Journal of Applied Physiology 2007;23(2):138-142
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the effect of extract of ginkgo biloba (EGb) and quercetin (Que) on the hypertrophic response induced by angiotensin II (Ang II) in the primary culture of neonatal rat cardiomyocytes and its mechanism.
METHODSTotal protein content of cardiomyocytes was measured by lowry's method. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured by SOD and MDA assay kits. The expression of phospho-ERK1/2, phospho-JNK and phospho-P38 were detected by Western blot. The expression of c-fos mRNA was checked by RT-PCR.
RESULTS(1) The total protein content and cell size of cardiomyocytes increased significantly after Ang II treatment, EGb and Oue inhibited these effects of Ang II. (2) EGb and Que were able to enhance the SOD activity and reduce the production of MDA. (3) Ang II significantly activated ERK1/2, JNK and P38, only JNK activation was inhibited by Que and DPI but not ERK1/2 and P38 activation. (4) EGb, Que, Captopril and DPI all decreased Ang II-stimulated early response gent c-fos mnRNA expression.
CONCLUSIONEGb and Que could inhibit AngII-induced cardiomyocyte hypertrophy through a ROS-dependent pathway, the effect of Que might be related to the JNK and c-fos cascade.
