Reduced cerebral ischemia-reperfusion injury in Toll-like receptor 4 deficient mice

Biochem Biophys Res Commun. 2007 Feb 9;353(2):509-14. doi: 10.1016/j.bbrc.2006.12.057. Epub 2006 Dec 18.

Abstract

Inflammatory reaction plays an important role in cerebral ischemia-reperfusion injury, however, its mechanism is still unclear. Our study aims to explore the function of Toll-like receptor 4 (TLR4) in the process of cerebral ischemia-reperfusion. We made middle cerebral artery ischemia-reperfusion model in mice with line embolism method. Compared with C3H/OuJ mice, scores of cerebral water content, cerebral infarct size and neurologic impairment in C3H/Hej mice were obviously lower after 6 h ischemia and 24 h reperfusion. Light microscopic and electron microscopic results showed that cerebral ischemia-reperfusion injury in C3H/Hej mice was less serious than that in C3H/OuJ mice. TNF-alpha and IL-6 contents in C3H/HeJ mice were obviously lower than that in C3H/OuJ mice with ELISA. The results showed that TLR4 participates in the process of cerebral ischemia-reperfusion injury probably through decrease of inflammatory cytokines. TLR4 may become a new target for prevention of cerebral ischemia-reperfusion injury. Our study suggests that TLR4 is one of the mechanisms of cerebral ischemia-reperfusion injury besides its important role in innate immunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / blood supply
  • Brain / metabolism
  • Brain / pathology
  • Brain Ischemia / metabolism*
  • Brain Ischemia / pathology*
  • Cerebral Infarction / metabolism*
  • Cerebral Infarction / pathology*
  • Female
  • Mice
  • Mice, Inbred C3H
  • Mice, Knockout
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / pathology*
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism*

Substances

  • Tlr4 protein, mouse
  • Toll-Like Receptor 4