Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

Seung Min Park; Chan Woo Park; Tae-Kyeong Lee; Jeong Hwi Cho; Joon Ha Park; Jae-Chul Lee; Bai Hui Chen; Bich-Na Shin; Ji Hyeon Ahn; Hyun-Jin Tae; Myoung Cheol Shin; Taek Geun Ohk; Jun Hwi Cho; Moo-Ho Won; Soo Young Choi; In Hye Kim

doi:10.4103/1673-5374.187039

Effect of ischemic preconditioning on antioxidant status in the gerbil hippocampal CA1 region after transient forebrain ischemia

Neural Regen Res. 2016 Jul;11(7):1081-9. doi: 10.4103/1673-5374.187039.

Authors

Affiliations

¹ 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.
² Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
³ Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea.
⁴ Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea.
⁵ Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea.

Abstract

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.

Keywords: antioxidant enzymes; hippocampus; ischemic preconditioning; nerve regeneration; neural regeneration; neuroprotection; pyramidal neurons; transient forebrain ischemia.