[Effect of HSP72 on acute injury of neonatal cardiomyocytes induced by oxidative stress].
OBJECTIVE
To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress.


METHODS
Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.5 mmol/L (final concentration) H2O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyocytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats.


RESULTS
Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP7-2 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2.


CONCLUSIONS
HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.
Luo
Xue-bing
XB
Cell Biology Research Laboratory, Xiangya School of Medicine, Central South University, Changsha, China. luoxuebing@126.com
Liu
Ke
K
Yi
Yu-xin
YX
Wang
Hao
H
Liu
Mei-dong
MD
Xiao
Xian-zhong
XZ
Deng
Gong-hua
GH
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D050884:HSP72 Heat-Shock Proteins / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000473:pathology*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D018384:Oxidative Stress; D014176:Protein Biosynthesis; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
D050884:HSP72 Heat-Shock Proteins; D016376:Oligonucleotides, Antisense; D007770:L-Lactate Dehydrogenase