Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury? | Zendy

Fenfei Gao | Zendy; Qiangyong Jia | Zendy; Fuxiao Guo | Zendy; Yanmei Zhang | Zendy; Zhanqin Huang | Zendy; Yanqiong Zhou | Zendy; Yicun Chen | Zendy; Ganggang Shi | Zendy

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Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Author(s) -

Fenfei Gao,

Qiangyong Jia,

Fuxiao Guo,

Yanmei Zhang,

Zhanqin Huang,

Yanqiong Zhou,

Yicun Chen,

Ganggang Shi

Publication year - 2009

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000257497

Subject(s) - lactate dehydrogenase , myeloperoxidase , cardioprotection , chemistry , malondialdehyde , pharmacology , reperfusion injury , troponin i , western blot , tumor necrosis factor alpha , creatine kinase , ischemia , inflammation , endocrinology , medicine , oxidative stress , biochemistry , enzyme , myocardial infarction , gene

Our previous studies have shown that N-n-butyl haloperidol iodide (F(2)) can antagonize myocardial ischemia/reperfusion (I/R) injury by blocking intracellular Ca(2+) overload and suppressing Egr-1 overexpression. The present study is to investigate the relation between the reduction of Ca(2+) overload and the inhibition of Egr-1 overexpression.

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