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 
[Ca(2+)](i), curtailment of the time from the maximum concentration of Ca(2+) to 
the baseline level and increased reuptake of Ca(2+) 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.