Isoflurane reduces hypoxia/reoxygenation-induced apoptosis and mitochondrial permeability transition in rat primary cultured cardiocytes

BMC Anesthesiology

Research Article

Wanjun Wu¹  Weidong Fei¹  Li Li¹  Ping Liu¹  Huifang Yun¹  Xianju Zhou² 

[1] Department of Anesthesiology, Changzhou No.2 People’s Hospital, the affiliated hospital of Nanjing Medical University, 213003, Changzhou, China;Department of Neurology, Changzhou No.2 People’s Hospital, the affiliated hospital of Nanjing Medical University, 213003, Changzhou, China;

关键词: Isoflurane;    Hypoxia/reoxygenation;    Cardiocyte;    Apoptosis;    Mitochondrial permeability transition;    ROS;   

DOI  :  10.1186/1471-2253-14-17

 received in 2013-09-23, accepted in 2014-03-03,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundThe volatile anesthetic isoflurane protects the heart from hypoxia/reperfusion (H/R) injury. However, it is still incompletely understood whether isoflurane exerts its protective role through preventing mitochondrial permeability transition pore (MPTP) opening.MethodsPrimary cultured cardiocytes were exposed to H/R in the absence or presence of isoflurane. Cell cytotoxicity and apoptosis were detected by MTT assay and TUNEL staining, respectively. MPTP function was monitored by confocal imaging after reoxygenation. ROS production and activation of caspase-3 were determined by fluorescent reader and western blot, respectively.ResultsAs compared to the control group, H/R led to significant cell cytotoxicity and apoptosis, while application of isoflurane markedly reversed the effects. Furthermore, isoflurane significantly inhibits the formation of H/R-induced excess ROS production. Finally, isoflurane attenuated the onset of mitochondrial permeability transition pore (MPTP) occurred during hypoxia/reoxygenation, and in turn inhibited activation of caspase-3.ConclusionsThese data indicate that isoflurane has a protective effect on cardiocytes exposed to H/R by reducing excess ROS production, blocking open of MPTP and further reducing apoptosis.

【 授权许可】

Unknown   
© Wu et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.