Suppression of oxidative stress after transient focal ischemia in interleukin-1 knock out mice

H. Ohtaki, A. Takaki, L. Yin, K. Dohi, T. Nakamachi, M. Matsunaga, R. Horai, M. Asano, Y. Iwakura, S. Shioda

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Abstract

Interleukin-l (IL-1) contributes to ischemic neurodegeneration. However, the mechanisms regulating action of IL-1 are still poorly understood. In order to clarify this central issue, mice that were gene deficient both IL-1α and β (IL-1 KO) and wild-type mice were subjected to 1 hour transient middle cerebral artery occlusion (tMCAO). The concentration of 8-hydroxy deoxyguanosine (80HdG) which is considered to be a reliable oxidative DNA damage by superoxide anion, in brain and of total nitric oxide (NO) in plasma were determined by use of HPLC. Twenty-four hours after tMCAO, the ratio of 80HdG to dG in the ipsilateral hemisphere of wild-type mice were 2.24 × 10 -3 and 4.41 × 10-3 in the neocortex and striatum, respectively. The concentration of 80HdG in the ipsilateral hemisphere of the wild-type mice was higher than that of the IL-1 KO mice. The concentration of total NO in the plasma of IL-1 KO mice was also lower than that of the wild-type 24 hours after tMCAO. These results strongly suggest that IL-1 is participated in generating reactive oxygen spices and it aggravates and induces the ischemic neuronal cell death. (183 words)

Original languageEnglish
Pages (from-to)191-194
Number of pages4
JournalActa Neurochirurgica, Supplementum
Issue number86
DOIs
Publication statusPublished - 2003

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology

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    Ohtaki, H., Takaki, A., Yin, L., Dohi, K., Nakamachi, T., Matsunaga, M., Horai, R., Asano, M., Iwakura, Y., & Shioda, S. (2003). Suppression of oxidative stress after transient focal ischemia in interleukin-1 knock out mice. Acta Neurochirurgica, Supplementum, (86), 191-194. https://doi.org/10.1007/978-3-7091-0651-8_41