Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia  

作　　者：Hyun-Jin Tae Il Jun Kang Tae-Kyeong Lee Jeong Hwi Cho Jae-Chul Lee Myoung Cheol Shin Yoon Sung Kim Jun Hwi Cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah Lee Yang Hee Kim Moo-Ho Won Young Joo Lee 

机构地区：[1]Bio-Safety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, South Korea [2]Department of Food Science and Nutrition, Hallym University, Chuncheon, South Korea [3]Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea [4]Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea [5]Department of Emergency Medicine, Samcheok Medical Center, Samcheok, South Korea [6]Division of Food Biotechnology, School of Biotechnology, Kangwon National University, Chuncheon, South Korea [7]Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea [8]Department of Obstetrics and Gynecology, School of Medicine, Kangwon National University, Chuncheon, South Korea [9]Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea [10]Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University, Seoul, South Korea

出　　处：《Neural Regeneration Research》2017年第12期2007-2013,共7页中国神经再生研究（英文版）

基　　金：supported by the Basic Science Research Program through the National Research Foundation of Korea(NRF);the Ministry of Education(NRF-2014R1A1A2057263);by the Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Science,ICT&Future Planning(NRF-2017R1A2B4009079&NRF-2017R1A2B4008403);by the Bio-Synergy Research Project(NRF-2015M3A9C4076322)of the Ministry of Science;ICT and Future Planning through the National Research Foundation

摘　　要：Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

关 键 词：nerve regeneration post-cardiac arrest syndrome NORMOTHERMIA neuronal damage GLIOSIS tumor necrosis factor-alpha neural regeneration 

分 类 号：R741[医药卫生—神经病学与精神病学]