Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia  

作　　者：In Hye Kim Yong Hwan Jeon Tae-Kyeong Lee Jeong Hwi Cho Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Bich-Na Shin Yang Hee Kim Seongkweon Hong Bing Chun Yan Moo-Ho Won Yun Lyul Lee 

机构地区：[1]Department of Neurobiology, School of Medicine, Kangwon National University [2]Department of Radiology, School of Medicine, Kangwon National University [3]Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University [4]Department of Physiology, College of Medicine, Hallym University [5]Department of Surgery, School of Medicine, Kangwon National University [6]Institute of Integrative Traditional & Western Medicine, Medical College, Yangzhou University

出　　处：《Neural Regeneration Research》2017年第6期918-924,共7页中国神经再生研究（英文版）

基　　金：supported by Hallym University Research Fund,2016(HRF-201605-012);Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(NRF-2016R1A6A3A01011698)

摘　　要：Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning（2-minute transient cerebral ischemia） on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult（5-minute transient cerebral ischemia）. A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28 k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning（2-minute transient cerebral ischemia） on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult（5-minute transient cerebral ischemia）. A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28 k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.

关 键 词：hippocampal subsequent minute pyramidal maintaining attenuated hippocampus neuronal occlusion fatal 

分 类 号：R743[医药卫生—神经病学与精神病学]