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Propofol protects the cardiomyocytes against hypoxia injury through inhibition of ER‐dependent apoptotic pathways
Author(s) -
Lai Hui Chin,
Liu Tsun-Jui,
Lee Hsiao-Wei,
Wang Li-Chuan,
Yeh Yueh-Chiao
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1117.4
Subject(s) - atf6 , apoptosis , unfolded protein response , propofol , hypoxia (environmental) , endoplasmic reticulum , chop , pharmacology , myocyte , medicine , microbiology and biotechnology , blot , cytochrome c , chemistry , biology , biochemistry , gene , organic chemistry , oxygen
Recent observations indicate that in the heart, the UPR is activated during acute stresses that lead to cardiac hypertrophy and heart failure. Hypoxia was found to mediate UPR activation in cardiac myocytes in vitro. This study was designed to examine whether propofol, an anesthetic with pluripotent cytoprotective properties, could ameliorate reduce the endoplasmic reticulum (ER) stress and hypoxia‐induced cardiomycytes apoptosis. Propofol pretreatment ameliorates apoptosis of hypoxia on cardiomyocytes. By using of immunofluorescence, western blotting analysis and RealTime‐PCR, propofol pretreatment were reduced mRNA expression of the crucial ER stress sensors ATF6, reduced pro‐apoptotic transcriptional factor C/EBP homologous protein (CHOP) and glucose‐regulated protein 78 (GRP78) and leads to apoptotic cell death. Our data has shown that propofol can ameliorate ER stress‐induced cardiac UPR‐reproducted and cardiomyocytes apoptosis. The effect of propofol may provide a new therapy to prevent the cardiovascular damage in stroke patients.