一氧化碳释放分子通过提高线粒体活性减轻复苏后大鼠的神经功能损伤

目的:探讨一氧化碳释放分子对心脏骤停并复苏后大鼠神经功能损伤的治疗作用及其机制。方法:建立大鼠窒息法心脏骤停模型,窒息时间约为11分钟,其中心脏骤停时间为6分钟。动物随机分为3组:假手术组;心脏骤停组;心脏骤停复苏后一氧化碳干预组。分别对复苏后的三组大鼠进行神经功能评分、脑海马组织TUNEL凋亡检测,脑ATP含量检测,线粒体呼吸和线粒体膜电位检测分析。结果:大鼠复苏后神经功能评分显著降低并且神经细胞发生大量凋亡,一氧化碳干预组大鼠相比未干预的大鼠,其神经功能评分显著提高,并且其大脑ATP含量、线粒体呼吸及膜电位也显著增强。结论:一氧化碳释放分子通过增强复苏后大鼠脑内线粒体活性而降低大鼠的神经功能损伤。

Carbon monoxide releasing molecules alleviate neurological injury after resuscitation of the rats through increasing brain mitochondrial activity

Objectives： To investigate the therapeutic effects and mechanism of carbon monoxide releasing molecules （CORM） on brain injury after cardiac arrest and resuscitation of the rats. Methods： A rat model of cardiac arrest was established by asphyxia, and asphyxia time is about 11 minutes, including cardiac arrest time was 6 minutes. The animals were randomly divided into throe groups：sham group; cardiac arrest group; cardiac arrest plus carbon monoxide intervention group. Three groups of rats were analyzed after successful resuscitation, including neurological function score, hippocampus tissue TUNEL apoptosis, cerebral ATP content, mitochondrial respiration and mitochondrial membrane potential. Results： The neurological function scores were significantly decreased after resuscitation and a large number of neurons had apoptosis. Compared to non-carbon monoxide treated animals, CO interventions were significantly increased neurological score, the brain ATP content, mitochondrial respiration and membrane potential. Conclusion： Carbon monoxide releasing molecules alleviate brain injury after resuscitation of the rats through increasing brain mitochondrial activity.