Inhibition of TNFalpha attenuates infarct volume and ICAM-1 expression in ischemic mouse brain.
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.
Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor 48109, USA.
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Yang
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Qin
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Bertz
D000818:Animals; D000911:Antibodies, Monoclonal; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D001831:Body Temperature / Q000187:drug effects; D002545:Brain Ischemia / Q000134:cerebrospinal fluid / Q000378:metabolism* / Q000473:pathology; D002544:Cerebral Infarction / Q000134:cerebrospinal fluid / Q000473:pathology*; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D017078:Laser-Doppler Flowmetry; D008297:Male; D051379:Mice; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000911:Antibodies, Monoclonal; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1