Article Publish Status: FREE
Abstract Title:

Eriodictyol Attenuates Myocardial Ischemia-Reperfusion Injury through the Activation of JAK2.

Abstract Source:

Front Pharmacol. 2018 ;9:33. Epub 2018 Jan 30. PMID: 29441020

Abstract Author(s):

Defang Li, Ning Lu, Jichun Han, Xiaoyu Chen, Wenjin Hao, Wenjuan Xu, Xiaona Liu, Lei Ye, Qiusheng Zheng

Article Affiliation:

Defang Li


Myocardial ischemia-reperfusion (I/R) injury remains the leading risk factor of disability and mortality worldwide. In this study, the myocardial protective effect of eriodictyol (EDT) and the underlying mechanism in anmodel of global myocardial I/R was investigated. After treatment with different concentrations of EDT, the decreased hemodynamic parameters induced by myocardial I/R injury were significantly attenuated by EDT. The elevated levels of IL-6, CRP, IL-8, and TNF-α were effectively reduced by EDT treatment. EDT also remarkably suppressed the levels of Bax and cleaved Caspase-3, and up-regulated the level of Bcl-2 in cardiac tissues from EDT-treated groups. Further studies showed that EDT could increase the levels of p-JAK2 and p-STAT3 in cardiac tissues. Meanwhile, treatment of AG490, a specific inhibitor of JAK2, abolished the protective effect of EDT on hemodynamic parameters, myocardial inflammation and myocardial cell apoptosis induced by I/R injury. These results demonstrated that EDT could protect against myocardial I/R injury through the activation of JAK2, providing a potential treatment with EDT during myocardial I/R injury.

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