Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury.
Mol Med Rep
; 16(2): 2290-2294, 2017 Aug.
Article
em En
| MEDLINE
| ID: mdl-28656215
ABSTRACT
Syringic acid (SA), a naturally occur-ring Omethy-lated trihydroxybenzoic acid monomer extracted from Dendrobium nobile Lindl., has been demonstrated to attenuate renal ischemiareperfusion (I/R) injury. However, the role of SA in myocardial I/R injury is unclear. The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. In the present study, it was revealed that pretreatment with SA increased the viability and inhibited oxidant stress in H9c2 cardiomyocytes that had suffered hypoxia/reoxygenation (H/R). SA also markedly downregulated Bcell lymphoma 2 (Bcl2) expression and inhibited the expression of Bcl2like protein 4 (Bax) and cleaved caspase3 in H9c2 cardiomyocytes induced by H/R. In addition, SA significantly alleviated H/R-induced the phosphorylation of p38 mitogenactivated protein kinase (p38MAPK) and cJun Nterminal kinase (JNK) in H9c2 cardiomyocytes. In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. The results support the therapeutic usage of SA in the treatment of myocardial infarction.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Transdução de Sinais
/
Hipóxia Celular
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Regulação para Baixo
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Apoptose
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Ácido Gálico
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article