Edema Formation Exacerbates Neurological and Histological Outcomes after Focal Cerebral Ischemia in CuZn-Superoxide Dismutase Gene Knockout Mutant Mice

T. Kondo, A. G. Reaume, T. T. Huang, K. Murakami, E. Carlson, S. Chen, R. W. Scott, C. J. Epstein, P. H. Chan

研究成果: Article査読

54 被引用数 (Scopus)

抄録

In a variety of studies, CuZn-superoxide dismutase (CuZn-SOD) has been shown to protect against ischemic brain injury. A possible role for CuZn-SOD-related modulation of neuronal viability has been suggested by the finding that CuZn-SOD inhibits brain edema formation following various kinds of neurological insults. We have evaluated the role of CuZn-SOD on brain edema formation following focal cerebral ischemia in mice bearing a disruption of the CuZn-SOD gene (Sod1). Homozygous mutants (Sod1+2) had no detectable CuZn-SOD activity and heterozygous mutants (Sod1+2) showed a 50% decrease compared to wild-type mice. Sod1+2 mice showed a high level of blood-brain barrier (BBB) disruption shortly after 1 hr of middle cerebral artery occlusion and 100% mortality at 24 hr following ischemia. Sod1+2 mice showed a moderate level of BBB disruption and 30% mortality. The Sod1+2 animals had increased infarct volume and brain swelling, accompanying exacerbated neurological deficits at 24 hr following ischemia. These results indicate the important role of superoxide anions in the development of brain edema after local cerebral ischemia and suggest the possibility that brain edema formation may contribute to the exacerbation of ischemic brain injury and neurological deficits in knockout mutant mice.

本文言語English
ページ(範囲)62-64
ページ数3
ジャーナルActa Neurochirurgica, Supplement
1997
70
DOI
出版ステータスPublished - 1997

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

フィンガープリント 「Edema Formation Exacerbates Neurological and Histological Outcomes after Focal Cerebral Ischemia in CuZn-Superoxide Dismutase Gene Knockout Mutant Mice」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル