This study examined the activation of mitophagy following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) and the relationship between the change with time and apoptosis. MAIN METHODS The male Sprague-Dawley rats were randomized into four groups: Sham group, CPR24h group, CPR48h group, CPR72h group. The rat model of cardiac arrest was established by asphyxiation. We employed western blot to analyze the levels of mitophagy related proteins of hippocampus, JC-1 to detect mitochondrial membrane potential (MMP) and flow cytometry to measure the rate of apoptosis of hippocampal neurons. Moreover, we also intuitively observed the occurrence of mitophagy through electron microscopy. KEY FINDINGS The results showed that the levels of TOMM20 and Tim23 protein were significantly decreased after CPR, which were more remarkable following 72 h of CPR. However, the protein levels of dynamin related protein 1 (Drp1) and cytochrome C (Cyt-c) were strongly up-regulated after CPR. Meanwhile, the hippocampal MMP decreased gradually with time after CPR. Furthermore, we more intuitively verified the activation of mitophagy through electron microscopy. In addition, the rats of apoptosis rate of hippocampus after CPR were significantly increased, which were gradually enhanced over time from 24 h until at least 72 h following CPR. SIGNIFICANCE with the enhancement of mitophagy, the apoptosis of hippocampal neurons was gradually enhanced, which suggested mitophagy may be excessive activated and aggravating brain damage after CA and CPR.

中文翻译：

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在心脏骤停和心肺复苏后，海马中的线粒体被过度激活。

这项研究检查了心脏骤停（CA）和心肺复苏（CPR）后线粒体的激活以及时间变化与凋亡之间的关系。主要方法将雄性Sprague-Dawley大鼠随机分为四组：假手术组，CPR24h组，CPR48h组，CPR72h组。通过窒息建立心脏骤停的大鼠模型。我们采用蛋白质印迹法分析了海马线粒体相关蛋白的水平，JC-1检测线粒体膜电位（MMP），流式细胞仪检测海马神经元的凋亡率。此外，我们还通过电子显微镜直观地观察到了线粒体的发生。主要结果结果表明，心肺复苏后，TOMM20和Tim23蛋白水平显着降低，心肺复苏72小时后更为明显。但是，在进行心肺复苏后，发电机相关蛋白1（Drp1）和细胞色素C（Cyt-c）的蛋白水平强烈上调。同时，心肺复苏后海马MMP随时间逐渐下降。此外，我们通过电子显微镜更直观地验证了线粒体的激活。此外，大鼠心肺复苏后海马细胞凋亡率显着增加，从24小时到至少72小时随时间逐渐增强。随着线粒体功能的增强，海马神经元的凋亡逐渐增强，提示线粒体功能可能被过度激活并加重了CA和CPR后的脑损伤。心肺复苏后，动力相关蛋白1（Drp1）和细胞色素C（Cyt-c）的蛋白水平上调。同时，心肺复苏后海马MMP随时间逐渐下降。此外，我们通过电子显微镜更直观地验证了线粒体的激活。此外，大鼠心肺复苏后海马细胞凋亡率显着增加，从24小时到至少72小时随时间逐渐增强。随着线粒体功能的增强，海马神经元的凋亡逐渐增强，提示线粒体功能可能被过度激活并加重了CA和CPR后的脑损伤。心肺复苏后，动力相关蛋白1（Drp1）和细胞色素C（Cyt-c）的蛋白水平上调。同时，心肺复苏后海马MMP随时间逐渐下降。此外，我们通过电子显微镜更直观地验证了线粒体的激活。此外，大鼠心肺复苏后海马细胞凋亡率显着增加，从24小时到至少72小时随时间逐渐增强。随着线粒体功能的增强，海马神经元的凋亡逐渐增强，提示线粒体功能可能被过度激活并加重了CA和CPR后的脑损伤。此外，大鼠心肺复苏后海马细胞凋亡率显着增加，从24小时到至少72小时随时间逐渐增强。随着线粒体功能的增强，海马神经元的凋亡逐渐增强，提示线粒体功能可能被过度激活并加重了CA和CPR后的脑损伤。此外，大鼠心肺复苏后海马的凋亡率显着增加，并且从心肺复苏后24小时到至少72小时随时间逐渐增强。随着线粒体功能的增强，海马神经元的凋亡逐渐增强，提示线粒体功能可能被过度激活并加重了CA和CPR后的脑损伤。