Jang Yoon-Sun, Lee Yo-Seob, Kim Dong-Hee, Oh Goo Taeg, Jeon Won Kyung, Han Jung-Soo
Department of Biological Science, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Division of Molecular Life Sciences, Ewha W. University, Seoul 03760, Republic of Korea.
Brain Res Bull. 2022 Jun 15;184:99-105. doi: 10.1016/j.brainresbull.2022.04.004. Epub 2022 Apr 20.
Peroxiredoxin 2 (Prx2) regulates oxidative stress response in neuronal injury. The present study examined the effects of Prx2 deletion on transient global ischemia-induced hippocampal-dependent memory impairment. First, 20-min bilateral common carotid artery occlusion (BCCAO)-reperfusion and sham-operated control procedures were conducted in 6- or 7-month-old Prx2 knockout and wild-type mice. The cognitive status of these mice was assessed using the Morris water maze task with a hidden platform and a novel object recognition task 7 days after the 20-min BCCAO. Next, to evaluate neuronal degeneration and oxidative stress in the CA1 subregion of the hippocampus critical for learning and memory, we measured immunoreactive Fluoro-jade C (FJC)-positive signals and 4-hydroxy-2-trans-nonenal (4-HNE) levels, respectively. The 20-min BCCAO induced cognitive impairments and increased the intensity of FJC-positive signals and 4-HNE levels of CA1 in Prx2 knockout mice but not in wild-type mice. These results suggest that Prx2 deficiency reduces resilience to transient global ischemia.
过氧化物酶体增殖物激活受体2（Prx2）调节神经元损伤中的氧化应激反应。本研究检测了Prx2基因缺失对短暂性全脑缺血诱导的海马依赖性记忆障碍的影响。首先，对6或7月龄的Prx2基因敲除小鼠和野生型小鼠进行20分钟的双侧颈总动脉闭塞（BCCAO）-再灌注及假手术对照操作。在20分钟BCCAO术后7天，使用带有隐藏平台的莫里斯水迷宫任务和新物体识别任务评估这些小鼠的认知状态。接下来，为了评估对学习和记忆至关重要的海马CA1亚区的神经元变性和氧化应激，我们分别测量了免疫反应性氟玉红C（FJC）阳性信号和4-羟基-2-反式壬烯醛（4-HNE）水平。20分钟的BCCAO诱导了Prx2基因敲除小鼠的认知障碍，并增加了CA1区FJC阳性信号的强度和4-HNE水平，但在野生型小鼠中未出现这种情况。这些结果表明，Prx2缺乏会降低对短暂性全脑缺血的恢复能力。
