Kim In Hye, Jeon Yong Hwan, Lee Tae-Kyeong, Cho Jeong Hwi, Lee Jae-Chul, Park Joon Ha, Ahn Ji Hyeon, Shin Bich-Na, Kim Yang Hee, Hong Seongkweon, Yan Bing Chun, Won Moo-Ho, Lee Yun Lyul
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Department of Radiology, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Neural Regen Res. 2017 Jun;12(6):918-924. doi: 10.4103/1673-5374.208573.
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 D28k 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.
由非致命性短暂血流阻断引发的缺血预处理已被用作一种针对后续致命性缺血损伤的实验性治疗策略。在本研究中,我们调查了缺血预处理(2分钟短暂性脑缺血)对沙土鼠海马CA1区在随后的致命性短暂缺血损伤(5分钟短暂性脑缺血)后钙结合蛋白D28k免疫反应性的神经保护作用。5分钟短暂性脑缺血后4天,海马CA1区大量锥体细胞死亡。缺血预处理减少了海马CA1区锥体细胞的死亡。钙结合蛋白D28k免疫反应性在5分钟短暂性脑缺血后2天大大减弱,在缺血后5天几乎检测不到。缺血预处理在短暂性脑缺血后维持了钙结合蛋白D28k免疫反应性。这些发现表明,缺血预处理可通过维持钙结合蛋白D28k免疫反应性减轻短暂性脑缺血对海马CA1区锥体细胞造成的损伤。