<i>N</i>-n-butyl Haloperidol Iodide Protects Cardiac Microvascular Endothelial Cells From Hypoxia/Reoxygenation Injury by Down-Regulating Egr-1 Expression
Author(s) -
Yanqiong Zhou,
Yanmei Zhang,
Fenfei Gao,
Fuxiao Guo,
Jinzhi Wang,
Wenfeng Cai,
Yicun Chen,
Jinhong Zheng,
Ganggang Shi
Publication year - 2010
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 - 10.1159/000323993
Subject(s) - lactate dehydrogenase , malondialdehyde , reperfusion injury , viability assay , western blot , superoxide dismutase , endothelial stem cell , chemistry , hypoxia (environmental) , endothelium , microbiology and biotechnology , pharmacology , andrology , biology , ischemia , medicine , oxidative stress , endocrinology , apoptosis , biochemistry , enzyme , in vitro , oxygen , organic chemistry , gene
Our previous studies have shown that N-n-butyl haloperidol iodide (F2) can antagonize myocardial ischemia/reperfusion (I/R) injury by down-regulating the early growth response (Egr)-1 expression, but the molecular mechanisms are not well understood. Because there is evidence implicating myocardial I/R injury is closely associated with endothelial dysfunction. The present study is to test the hypothesis that the protective effects of F2 on myocardial I/R injury is related closely with down-regulating Egr-1 expression on cardiac microvascular endothelial cells (CMECs).
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