Neurochemical Research

, Volume 37, Issue 2, pp 307–313

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Authors

  • Woosuk Kim
    • Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary ScienceSeoul National University
  • Dae Won Kim
    • Department of Biomedical Sciences, and Research Institute for Bioscience and BiotechnologyHallym University
  • Dae Young Yoo
    • Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary ScienceSeoul National University
  • Jin Young Chung
    • Department of NeurologySeoul National University Hospital
  • In Koo Hwang
    • Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary ScienceSeoul National University
  • Moo-Ho Won
    • Department of Neurobiology, School of MedicineKangwon National University
  • Soo Young Choi
    • Department of Biomedical Sciences, and Research Institute for Bioscience and BiotechnologyHallym University
  • Sei Woong Jeon
    • Department of Neurosurgery, Hangang Sacred Heart Hospital, College of MedicineHallym University
  • Je Hoon Jeong
    • Department of Neurosurgery, Hangang Sacred Heart Hospital, College of MedicineHallym University
  • Hyung Sik Hwang
    • Department of Neurosurgery, Hangang Sacred Heart Hospital, College of MedicineHallym University
    • Department of Neurosurgery, Hangang Sacred Heart Hospital, College of MedicineHallym University
Original Paper

DOI: 10.1007/s11064-011-0613-0

Cite this article as:
Kim, W., Kim, D.W., Yoo, D.Y. et al. Neurochem Res (2012) 37: 307. doi:10.1007/s11064-011-0613-0

Abstract

A rabbit model of spinal cord ischemia has been introduced as a good model to investigate the pathophysiology of ischemia–reperfusion (I–R)-induced paraplegia. In the present study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) against ischemic damage in the ventral horn of L5–6 levels in the rabbit spinal cord. For this study, the expression vector PEP-1 was constructed, and this vector was fused with SOD1 to create a PEP-1-SOD1 fusion protein that easily penetrated the blood–brain barrier. Spinal cord ischemia was induced by transient occlusion of the abdominal aorta for 15 min. PEP-1-SOD1 (0.5 mg/kg) was intraperitoneally administered to rabbits 30 min before ischemic surgery. The administration of PEP-1-SOD1 significantly improved neurological scores compared to those in the PEP-1 (vehicle)-treated ischemia group. Also, in this group, the number of cresyl violet-positive cells at 72 h after I–R was much higher than that in the vehicle-treated ischemia group. Malondialdehyde levels were significantly decreased in the ischemic spinal cord of the PEP-1-SOD1-treated ischemia group compared to those in the vehicle-treated ischemia group. In contrast, the administration of PEP-1-SOD1 significantly ameliorated the ischemia–induced reduction of SOD and catalase levels in the ischemic spinal cord. These results suggest that PEP-1-SOD1 protects neurons from spinal ischemic damage by decreasing lipid peroxidation and maintaining SOD and catalase levels in the ischemic rabbit spinal cord.

Keywords

Transient spinal ischemiaNeuroprotectionLipid peroxidationAntioxidants

Supplementary material

11064_2011_613_MOESM1_ESM.tif (12.1 mb)
Supplementary material 1 (TIFF 12371 kb). Neurological function scores by modified Tarlov criteria in the sham, PEP-1-ischemia and PEP-1-SOD1-ischemia groups at 24, 48, and 72 h after I-R

Copyright information

© Springer Science+Business Media, LLC 2011