Jang, Yoon-Sun Lee, Yo-Seob Kim, Dong-Hee Oh, Goo Taeg Jeon, Won Kyung Han, Jung-Soo 2024-01-19T12:01:28Z 2024-01-19T12:01:28Z 2022-05-27 2022-06 0361-9230 https://pubs.kist.re.kr/handle/201004/115157 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. English Elsevier BV Peroxiredoxin 2 deletion impairs hippocampal-dependent memory via exacerbating transient ischemia-induced oxidative damage Article 10.1016/j.brainresbull.2022.04.004 1 Brain Research Bulletin, v.184, pp.99 - 105 Brain Research Bulletin 184 99 105 N scie scopus 000794182700003 Neurosciences Neurosciences & Neurology Article CAROTID-ARTERY OCCLUSION CEREBRAL-ISCHEMIA FLUORO-JADE RECOGNITION MEMORY CA1 NEURONS INJURY RATS OVEREXPRESSION PROTECTS STRESS Peroxiredoxin 2 Transient global ischemia Hippocampus Memory Mice