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Ginkgo biloba extract EGB761 protects against aging-associated diastolic dysfunction in cardiomyocytes of D-galactose-induced aging rat.

Liu J, Wang J, Chen X, Guo C, Guo Y, Wang H - Oxid Med Cell Longev (2012)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Gerontology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.

ABSTRACT
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.

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Response of neonatal rat cardiomyocytes to 5 g·L−1 D-galactose and 5 g·L−1 D-galactose combined with 20 μg·mL−1 EGB761 for 48 h. Phase-contrast images showing morphologic changes and stained cells. (SA-β-gal positive cells; Blue, magnification ×400).
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fig1: Response of neonatal rat cardiomyocytes to 5 g·L−1 D-galactose and 5 g·L−1 D-galactose combined with 20 μg·mL−1 EGB761 for 48 h. Phase-contrast images showing morphologic changes and stained cells. (SA-β-gal positive cells; Blue, magnification ×400).

Mentions: Meanwhile, AGEs are considered as one of the important markers in cardiac aging. In the present study, AGEs content was significantly increased in the D-galactose-treated group. Significantly decreased AGEs level was observed in different concentrations of EGB761 treatment groups (n = 20 number of rats each group and n = 6 experimental replicates; P < 0.05 versus D-galactose) (Table 1 and Figure 1).


Ginkgo biloba extract EGB761 protects against aging-associated diastolic dysfunction in cardiomyocytes of D-galactose-induced aging rat.

Liu J, Wang J, Chen X, Guo C, Guo Y, Wang H - Oxid Med Cell Longev (2012)

Response of neonatal rat cardiomyocytes to 5 g·L−1 D-galactose and 5 g·L−1 D-galactose combined with 20 μg·mL−1 EGB761 for 48 h. Phase-contrast images showing morphologic changes and stained cells. (SA-β-gal positive cells; Blue, magnification ×400).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368694&req=5

fig1: Response of neonatal rat cardiomyocytes to 5 g·L−1 D-galactose and 5 g·L−1 D-galactose combined with 20 μg·mL−1 EGB761 for 48 h. Phase-contrast images showing morphologic changes and stained cells. (SA-β-gal positive cells; Blue, magnification ×400).
Mentions: Meanwhile, AGEs are considered as one of the important markers in cardiac aging. In the present study, AGEs content was significantly increased in the D-galactose-treated group. Significantly decreased AGEs level was observed in different concentrations of EGB761 treatment groups (n = 20 number of rats each group and n = 6 experimental replicates; P < 0.05 versus D-galactose) (Table 1 and Figure 1).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Gerontology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus