Park Seung Min, Park Chan Woo, Lee Tae-Kyeong, Cho Jeong Hwi, Park Joon Ha, Lee Jae-Chul, Chen Bai Hui, Shin Bich-Na, Ahn Ji Hyeon, Tae Hyun-Jin, Shin Myoung Cheol, Ohk Taek Geun, Cho Jun Hwi, Won Moo-Ho, Choi Soo Young, Kim In Hye
Department of Emergency Medicine, Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, South Korea; Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
Neural Regen Res. 2016 Jul;11(7):1081-9. doi: 10.4103/1673-5374.187039.
Ischemic preconditioning (IPC) is a condition of sublethal transient global ischemia and exhibits neuroprotective effects against subsequent lethal ischemic insult. We, in this study, examined the neuroprotective effects of IPC and its effects on immunoreactive changes of antioxidant enzymes including superoxide dismutase (SOD) 1 and SOD2, catalase (CAT) and glutathione peroxidase (GPX) in the gerbil hippocampal CA1 region after transient forebrain ischemia. Pyramidal neurons of the stratum pyramidale (SP) in the hippocampal CA1 region of animals died 5 days after lethal transient ischemia without IPC (8.6% (ratio of remanent neurons) of the sham-operated group); however, IPC prevented the pyramidal neurons from subsequent lethal ischemic injury (92.3% (ratio of remanent neurons) of the sham-operated group). SOD1, SOD2, CAT and GPX immunoreactivities in the sham-operated animals were easily detected in pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region, while all of these immunoreactivities were rarely detected in the stratum pyramidale at 5 days after lethal transient ischemia without IPC. Meanwhile, their immunoreactivities in the sham-operated animals with IPC were similar to (SOD1, SOD2 and CAT) or higher (GPX) than those in the sham-operated animals without IPC. Furthermore, their immunoreactivities in the stratum pyramidale of the ischemia-operated animals with IPC were steadily maintained after lethal ischemia/reperfusion. Results of western blot analysis for SOD1, SOD2, CAT and GPX were similar to immunohistochemical data. In conclusion, IPC maintained or increased the expression of antioxidant enzymes in the stratum pyramidale of the hippocampal CA1 region after subsequent lethal transient forebrain ischemia and IPC exhibited neuroprotective effects in the hippocampal CA1 region against transient forebrain ischemia.
缺血预处理（IPC）是一种亚致死性短暂全脑缺血状态，对随后的致死性缺血损伤具有神经保护作用。在本研究中，我们检测了IPC对沙土鼠前脑短暂缺血后海马CA1区抗氧化酶（包括超氧化物歧化酶（SOD）1和SOD2、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPX））免疫反应性变化的神经保护作用及其影响。在没有IPC的致死性短暂缺血后5天，动物海马CA1区锥体层（SP）的锥体神经元死亡（假手术组残留神经元比例为8.6%）；然而，IPC可防止锥体神经元遭受随后的致死性缺血损伤（假手术组残留神经元比例为92.3%）。在假手术动物海马CA1区锥体层（SP）的锥体神经元中很容易检测到SOD1、SOD2、CAT和GPX的免疫反应性，而在没有IPC的致死性短暂缺血后5天，在锥体层中几乎检测不到所有这些免疫反应性。同时，在接受IPC的假手术动物中，它们的免疫反应性与未接受IPC的假手术动物相似（SOD1、SOD2和CAT）或更高（GPX）。此外，在接受IPC的缺血手术动物的锥体层中，它们的免疫反应性在致死性缺血/再灌注后稳定维持。SOD1、SOD2、CAT和GPX的蛋白质印迹分析结果与免疫组织化学数据相似。总之，IPC在随后的致死性前脑短暂缺血后维持或增加了海马CA1区锥体层抗氧化酶的表达，并且IPC在海马CA1区对前脑短暂缺血具有神经保护作用。
