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Ginsenoside Re enhances the survival of H9c2 cardiac muscle cells through regulation of autophagy.
Zhang, Zi-Long; Liu, Mei-Lin; Huang, Ying-Shuo; Liang, Wen-Yi; Zhang, Miao-Miao; Fan, Yu-Dong; Ma, Ming-Feng.
Afiliação
  • Zhang ZL; Department of Cardiology, Emergency General Hospital, Beijing 100028, China.
  • Liu ML; Department of Geriatric, Peking University First Hospital, Beijing 100034, China.
  • Huang YS; Department of Research Ward, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
  • Liang WY; Department of Geriatric, Peking University First Hospital, Beijing 100034, China.
  • Zhang MM; Department of Cardiology, Emergency General Hospital, Beijing 100028, China.
  • Fan YD; Department of Cardiology, Emergency General Hospital, Beijing 100028, China.
  • Ma MF; Department of Cardiology, Fenyang Hospital of Shanxi Province, Fenyang 032200, China.
J Asian Nat Prod Res ; 22(8): 774-787, 2020 Aug.
Article em En | MEDLINE | ID: mdl-31232107
ABSTRACT
We examined the effect of ginsenoside Re (G-Re) on autophagy in H9c2 cardiomyocytes cultured in glucose deprivation (GD). Levels of the membrane-bound autophagy-related microtubule-associated protein 1A/1B-light chain 3 (LC3) B-2 were measured via immunoblotting and immunofluorescence was conducted to assess autophagosome formation. GD H9c2 cells were treated with 100 µmol/l G-Re. Cell viability was determined in culture medium. Phosphorylated 5' AMP-activated protein kinase (AMPK)-α and mammalian target of rapamycin (mTOR) levels were measured to explore the mechanisms underlying the effects of G-Re on autophagy in GD cells. G-Re treatment inhibited autophagosome formation and may be beneficial to GD cardiomyocytes.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Ginsenosídeos Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Ginsenosídeos Idioma: En Ano de publicação: 2020 Tipo de documento: Article