Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury | Zendy

Shoukun Ding | Zendy; Lixia Wang | Zendy; Lei-Sheng Guo | Zendy; Ping Luo | Zendy; Juanjuan Du | Zendy; Zonglei Zhao | Zendy; Guang-Gong Wang | Zendy

Open Access

Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury

Author(s) -

Shoukun Ding,

Lixia Wang,

Lei-Sheng Guo,

Ping Luo,

Juanjuan Du,

Zonglei Zhao,

Guang-Gong Wang

Publication year - 2017

Publication title -

molecular medicine reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.727

H-Index - 56

eISSN - 1791-3004

pISSN - 1791-2997

DOI - 10.3892/mmr.2017.6845

Subject(s) - apoptosis , p38 mitogen activated protein kinases , hypoxia (environmental) , kinase , reperfusion injury , chemistry , signal transduction , protein kinase a , mitogen activated protein kinase , downregulation and upregulation , pharmacology , ischemia , microbiology and biotechnology , biology , medicine , biochemistry , organic chemistry , oxygen , gene

Syringic acid (SA), a naturally occur-ring O‑methy-lated trihydroxybenzoic acid monomer extracted from Dendrobium nobile Lindl., has been demonstrated to attenuate renal ischemia‑reperfusion (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 B‑cell lymphoma 2 (Bcl‑2) expression and inhibited the expression of Bcl‑2‑like protein 4 (Bax) and cleaved caspase‑3 in H9c2 cardiomyocytes induced by H/R. In addition, SA significantly alleviated H/R-induced the phosphorylation of p38 mitogen‑activated protein kinase (p38MAPK) and c‑Jun N‑terminal 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.

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