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Improving effects of ginsenoside Rb1 on glucose metabolism in cardio-myocytes under hypoxia by hypoxia-inducible factor 1α / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 1621-1626, 2016.
Article in Chinese | WPRIM | ID: wpr-498656
ABSTRACT

AIM:

To elucidate the effect of ginsenoside Rb1 (Gs-Rb1) on the glucose metabolism to improve the viability of the cardiomyocytes under hypoxia, and whether hypoxia-inducible factor 1α(HIF-1α) and/or AMPKαare involved in the process.

METHODS:

The neonatal rat cardiomyocytes were cultured, and randomly divided into control group, hypoxia (1% O2 , 94% N2 and 5% CO2 ) group, Gs-Rb1 (200 μmol/L) group, Ara-A (500 μmol/L) group, Gs-Rb1 +Ara-A group, YC-1 (5 μmol/L) group, Gs-Rb1 +YC-1 group, Ara-A +YC-1 group and Gs-Rb1 +YC-1 +Ara-A group.After the intervention for 8 h, the cell viability was analyzed by MTT assay.The protein levels of AMPK, HIF-1αand glucose transporter-4 (GLUT-4) were determined by Western blot.The activities of heterophosphatase (HK), phos-phofructokinase (PFK) and lactic dehydrogenase (LDH) were measured by ELISA.

RESULTS:

Gs-Rb1 significantly im-proved the viability of hypoxic cardiomyocytes, which was significantly inhibited by YC-1 and Ara-A.In addition, YC-1 and Ara-A had a synergistic effect.Gs-Rb1 increased the protein levels of AMPK and HIF-1αin the hypoxic cardiomyo-cytes, which was significantly inhibited by Ara-A and YC-1.Gs-Rb1 significantly increased the expression of GLUT-4 on the cytomembrane of hypoxic cardiomyocytes, which was significantly inhibited by YC-1 or Ara-A, especially Ara-A +YC-1.Gs-Rb1 significantly increased the activities of HK, PFK and LDH, all those were significantly inhibited by YC-1 or Ara-A.Besides, YC-1 and Ara-A had a synergistic effect.

CONCLUSION:

Gs-Rb1 improves the viability of hypoxic car-diomyocytes, which may be related to the regulation of glucose uptake and enhancement of glycolysis by synergy of both HIF-1αand AMPK.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2016 Type: Article