Open AccessEgr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?
Author(s) -
Fenfei Gao,
Qiang-Yong Jia,
Fuxiao Guo,
Yanmei Zhang,
Zhanqin Huang,
Yanliang Zhou,
Yicun Chen,
GuoMing 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.