Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 66, Issue 1, Pages 57-63Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2011.11.014
Keywords
17 beta-Estradiol; Hydrogen peroxide; Bone marrow mesenchymal; Jun N-terminal kinases
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This study was designed to investigate the function of 17 beta-estradiol (17 beta-E2) against oxidative stress on the cell death of mice bone marrow mesenchymal stem cells (BMSCs) induced by hydrogen peroxide (H2O2). BMSCs were treated with 17 beta-E2 for 24 h and then treated with 100 mu M H2O2 for 1 h. Cell viability, apoptosis, caspase-9 mRNA, JNKs (Jun N-terminal kinases) and c-Jun protein expression in BMSCs were evaluated. Cell apoptosis of BMSCs were increased in a dose-dependent manner after treated with H2O2 compared to control group. But pretreatment with 17 beta-E-2 can inhibit apoptosis of BMSCs, preserve the mitochondrial transmembrane potential, decrease caspase-9 mRNA, JNK1/2 and c-un protein expression. In conclusion, 17 beta-E-2 exerts antiapoptotic effects in BMSCs which related to the mitochondria death pathway and JNKs pathway. The study revealed that 17 beta-E-2 can reduce the donor stem cells damage. Crown Copyright (C) 2012 Published by Elsevier Masson SAS. All rights reserved.
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