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Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
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Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
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Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo

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Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo
Journal Article

Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardio- myocytes is mediated through the specific activation of glucose transporter-4 ex vivo

2009
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Overview
Aim: The aim of this study was to investigate whether Gs-Rbl relieves the CoC12-induced apoptosis of hypoxic neonatal rat cardiomyocytes and in which the role of glucose transporter-4 (GLUT-4). Methods: Gs-Rbl (0, 10, 50, 100, 200, 400, and 500 μmol/L), adenine 9-β-D-arabinofuranoside (ara A, 500 μmol/L; AMPK inhibitor) and wortmannin (0.5μmol/L; PI3K inhibitor) only in combination with 200 μmol/L Gs-Rbl were administered in hypoxic cardiomyocytes, which were induced by 500μmol/L COCl2 for 12 h. Then, the apoptotic rate (AR), 2-[3H]-deoxy- D-glucose (2-[3H]-DG) uptake, and the expression of GLUT-4 (including in plasma membrane, PM), phospho-AMPKa (Thr172), AMPKa and Akt in cells were assayed. Results: Compared with simple hypoxia (0μmol/L Gs-Rbl), Gs-Rbl greater than 10μmol/L significantly decreased the apoptotic rate (P〈0.01) and significantly increased 2-[3H]-DG uptake (P〈0.01), GLUT-4 content in cells and PM (P〈0.01), AMPK activity (P〈0.01) and Akt (P〈0.01) levels in a dose-dependent manner. AMPK activity was completely suppressed by ara-A, just as Akt was suppressed by wortmannin. The AR, glucose uptake and GLUT-4 levels in cells and PM were partly down-regulated by ara-A or wortmannin. Conclusion: Gs-Rbl may protect neonatal rat cardiomyocytes from apoptosis induced by CoCl2. The anti-apoptotic effect of Gs-Rbl may occur by improving glucose uptake, in which GLUT-4 translocation and expression played a key role. Both the AMPK and the PI3K/Akt pathways may take part in the anti-hypoxic efficacy of Gs-Rbl.

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