Inhibition of TNFalpha attenuates infarct volume and ICAM-1 expression in ischemic mouse brain

Neuroreport. 1998 Jun 22;9(9):2131-4. doi: 10.1097/00001756-199806220-00041.

Abstract

The purpose of our study was to determine whether inhibiting the action of tumor necrosis factor-alpha (TNFalpha) attenuates brain injury and reduces inflammatory responses in the mouse during ischemia and reperfusion. Mice underwent middle cerebral artery occlusion (MCAO) for 1 h followed by 23 h reperfusion. Monoclonal neutralizing anti-murine TNFalpha antibody (mAb) was administrated intraventricularly in the mouse with temporary MCAO. Infarct volume in the anti-TNFalpha mAb treated mice was significantly smaller than that in the control group (p < 0.05). The number of intercellular adhesion molecule-1 (ICAM-1)-positive vessels in the ischemic area of the anti-TNFalpha mAb-treated group was significantly less than that in the control group. Our study demonstrated that blocking TNFalpha reduced brain injury and attenuated ICAM-1 expression during transient cerebral ischemia.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Blood Gas Analysis
  • Blood Pressure / drug effects
  • Body Temperature / drug effects
  • Brain Ischemia / cerebrospinal fluid
  • Brain Ischemia / metabolism*
  • Brain Ischemia / pathology
  • Cerebral Infarction / cerebrospinal fluid
  • Cerebral Infarction / pathology*
  • Immunohistochemistry
  • Intercellular Adhesion Molecule-1 / biosynthesis*
  • Laser-Doppler Flowmetry
  • Male
  • Mice
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*

Substances

  • Antibodies, Monoclonal
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1