Interleukin-1 in Cerebral Ischemia.

DOI Web Site PubMed 参考文献102件
  • Betz A Lorris
    Departments of Surgery Departments of Pediatrics and Neurology, University of Michigan
  • Schielke Gerald P
    Department of Neurological and Neurodegenerative Diseases, Parke-Davis Pharmaceutical Research, Division of the Warner-Lambert Company
  • Yang Guo-Yuan
    Departments of Surgery

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During the past several years, it has become increasingly apparent that interleukin-1 (IL-1), particularly IL-1β plays an important role in brain injury during ischemia. Studies from various laboratories have shown that IL-1β mRNA and IL-1β protein are synthesized early in ischemia and that the injection of IL-1β into ischemic brain enhances edema formation. The most direct evidence that IL-1β contributes to ischemic injury, however, is the demonstration that infarct volume in focal ischemia is reduced following intraventricular injection of an endogenous interleukin-1 receptor antagonist (IL-1ra), or after IL-lra is overexpressed in brain using an adenoviral vector to transfer IL-Ira cDNA to brain cells. Ischemic injury is also reduced in mice that fail to produce IL-1β because of an abnormal interleukin-1β converting enzyme gene (ICE knockout mice). At the present time, it is unclear how IL-1β causes brain injury, but several possible mechanisms include 1) stimulation of an inflammatory response through the activation of glia or the induction of other cytokines and/or endothelial adhesion molecules and 2) release of free radicals through stimulation of arachidonic acid metabolism and/or nitric oxide synthase activity.

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