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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 418748, 7 pages
Research Article

Ginkgo Biloba Extract EGB761 Protects against Aging-Associated Diastolic Dysfunction in Cardiomyocytes of D-Galactose-Induced Aging Rat

1Department of Gerontology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China
2Institute of Cardiovascular Disease, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China
3Department of Cardiology, Anyang Sixth People Hospital, Anyang, Henan 455000, China
4Department of Cardiology, The Shengze Hospital of Jiangsu Province, SuZhou 215002, China

Received 30 November 2011; Revised 6 March 2012; Accepted 13 March 2012

Academic Editor: Ana Fortuno

Copyright © 2012 Jing Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of the present study was to make use of the artificially induced aging model cardiomyocytes to further investigate potential anti-aging-associated cellular diastolic dysfunction effects of EGB761 and explore underlying molecular mechanisms. Cultured rat primary cardiomyocytes were treated with either D-galactose or D-galactose combined with EGB761 for 48 h. After treatment, the percentage of cells positive for SA-β-gal, AGEs production, cardiac sarcoplasmic reticulum calcium pump (SERCA) activity, the myocardial sarcoplasmic reticulum calcium uptake, and relative protein levels were measured. Our results demonstrated that in vitro stimulation with D-galactose induced AGEs production. The addition of EGB761 significantly decreased the number of cells positive for SA-β-gal. Furthermore, decreased diastolic [Ca2+]i, curtailment of the time from the maximum concentration of Ca2+ to the baseline level and increased reuptake of Ca2+ stores in the SR were also observed. In addition, the level of p-Ser16-PLN protein as well as SERCA was markedly increased. The study indicated that EGb761 alleviates formation of AGEs products on SERCA2a in order to mitigate myocardial stiffness on one hand; on other hand, improve SERCA2a function through increase the amount of Ser16 sites PLN phosphorylation, which two hands finally led to ameliorate diastolic dysfunction of aging cardiomyocytes.