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Apelin-APJ Effects of Ginsenoside-Rb1 Depending on Hypoxia-Induced Factor 1α in Hypoxia Neonatal Cardiomyocytes
  
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KeyWord:ginsenosides-Rb1, cardiomyocytes, hypoxia, apelin, APJ, hypoxia-induced factor 1α
Author NameAffiliationE-mail
KONG Hong-liang Cardiology Center, The People's Hospital of Liaoning Province, Shenyang (110016), China kh1339@sina.com 
LI Zhan-quan, ZHAO Shu-mei, YUAN Long   
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Abstract:
      Objective: To investigate whether ginsenoside-Rb1 (Gs-Rb1) inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α (Hif-1α). Methods: Neonatal rat cardiomyocytes were randomly divided into 6 groups: a control group, a simple CoCl2 group, a simple Gs-Rb1 group, a CoCl2 and Gs-Rb1 hypoxia group, a CoCl2 and 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) group, a CoCl2 and YC-1 group and a Gs-Rb1 group, in which YC-1 inhibits the synthesis and accelerates the degradation of Hif-1a. The concentration of CoCl2, Gs-Rb1 and YC-1 was 500 μmol/L, 200 μmol/L and 5 μmol/L, respectively; the apoptosis ratio was analyzed with a flow cytometer; and apelin, APJ and Hif-1α were assayed with immunocytochemistry, Western blot assays and reverse transcription polymerase chain reaction (RT-PCR). Results: (1) The anti-apoptosis effect of Gs-Rb1 on hypoxia cardiomyocytes was significantly inhibited by YC-1; (2) Hypoxia significantly up-graded the expression of mRNA and protein of apelin; this effect was further reinforced by Gs-Rb1 and significantly inhibited by YC-1; (3) Gs-Rb1 further strengthened the expression of APJ mRNA and APJ proteins once hypoxia occurred, which was significantly inhibited by YC-1; (4) Gs-Rb1 significantly increased the expression of Hif-1α, which was completely abolished by YC-1; (5) There was a negative relationship between AR and apelin (or APJ, including mRNA and protein), a positive correlation between apelin (or APJ) protein and Hif-1a protein, in hypoxia cardiomyocytes. Conclusion: The apelin-APJ system plays an important role in the anti-apoptosis effect of Gs-Rb1 on hypoxia neonatal cardiomyocytes, which was partly adjusted by Hif-1α.
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