Carbon Monoxide Improves Neurologic Outcomes by Mitochondrial Biogenesis after Global Cerebral Ischemia Induced by Cardiac Arrest in Rats.
Carbon Monoxide Improves Neurologic Outcomes by Mitochondrial Biogenesis after Global Cerebral Ischemia Induced by Cardiac Arrest in Rats.
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一氧化碳通过线粒体生物发生改善大鼠心脏骤停引起的全脑缺血后的神经系统结果
DOI：
10.7150/ijbs.13222
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发表时间：
2016
影响因子：
9.2
通讯作者：
Huang ZT
中科院分区：
文献类型：
--
作者：
Wang P;Yao L;Zhou LL;Liu YS;Chen MD;Wu HD;Chang RM;Li Y;Zhou MG;Fang XS;Yu T;Jiang LY;Huang ZT
线粒体功能障碍在心脏骤停后全脑缺血脑损伤中的作用一氧化碳治疗在缺血/再灌注损伤中显示出有效的细胞保护作用。本研究旨在探讨一氧化碳释放分子对大鼠心脏骤停复苏后脑线粒体功能障碍和脑损伤的影响。采用窒息法建立大鼠心脏骤停模型。将动物随机分为3组：心脏骤停复苏组、心脏骤停复苏加一氧化碳干预组和假手术对照组（无心脏骤停）。自主循环恢复后，神经功能缺损评分（NDS）和S-100 B水平在24、48和72 h均显著降低，但一氧化碳治疗可改善24 h NDS和S-100 B水平，并提高大鼠3 d存活率。这种治疗也减少了海马CA1区受损神经元的数量，并增加了脑线粒体活性。此外，它通过增加生物合成因子包括过氧化物酶体增殖物激活受体-γ共激活因子-1 α、核呼吸因子-1、核呼吸因子-2和线粒体转录因子A的表达来增加线粒体生物合成。因此，该研究表明，一氧化碳治疗通过增加脑线粒体生物合成减轻了大鼠心脏骤停后的脑损伤。
Mitochondrial dysfunction contributes to brain injury following global cerebral ischemia after cardiac arrest. Carbon monoxide treatment has shown potent cytoprotective effects in ischemia/reperfusion injury. This study aimed to investigate the effects of carbon monoxide-releasing molecules on brain mitochondrial dysfunction and brain injury following resuscitation after cardiac arrest in rats. A rat model of cardiac arrest was established by asphyxia. The animals were randomly divided into the following 3 groups: cardiac arrest and resuscitation group, cardiac arrest and resuscitation plus carbon monoxide intervention group, and sham control group (no cardiac arrest). After the return of spontaneous circulation, neurologic deficit scores (NDS) and S-100B levels were significantly decreased at 24, 48, and 72 h, but carbon monoxide treatment improved the NDS and S-100B levels at 24 h and the 3-day survival rates of the rats. This treatment also decreased the number of damaged neurons in the hippocampus CA1 area and increased the brain mitochondrial activity. In addition, it increased mitochondrial biogenesis by increasing the expression of biogenesis factors including peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, nuclear respiratory factor-2 and mitochondrial transcription factor A. Thus, this study showed that carbon monoxide treatment alleviated brain injury after cardiac arrest in rats by increased brain mitochondrial biogenesis.