Effect of anti-rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5 '-triphosphatase and superoxide dismutase activation, and ultrastructural changes


TUNA M. , POLAT S., Erman T. , ILDAN F. , GOCER A. İ. , TUNA N., et al.

JOURNAL OF NEUROSURGERY, cilt.95, ss.64-73, 2001 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 95 Konu: 1
  • Basım Tarihi: 2001
  • Doi Numarası: 10.3171/spi.2001.95.1.0064
  • Dergi Adı: JOURNAL OF NEUROSURGERY
  • Sayfa Sayısı: ss.64-73

Özet

Object. The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti-rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5 ' -triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment.