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

BMC Anesthesiology

Wanjun Wu²  Xianju Zhou¹  Ping Liu²  Weidong Fei²  Li Li²  Huifang Yun² 

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

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

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

Others  :  816493
DOI  :  10.1186/1471-2253-14-17

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

【 摘 要 】

Background

The 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.

Methods

Primary 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.

Results

As 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.

Conclusions

These 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】

   
2014 Wu et al.; licensee BioMed Central Ltd.

【 图 表 】

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