title: Dexamethasone attenuates early expression of three molecules associated with microglia/macrophages activation following rat traumatic brain injury.
abstract: Corticosteroids have been used in the treatment of human traumatic brain injury (TBI), which is a leading cause of death and disability, but their efficiency is still a matter of debate. Dexamethasone was considered to delay post-traumatic inflammation and retard neuronal degeneration, resulting in attenuation of secondary injury following experimental TBI. In a rat TBI model, we have investigated the effects of dexamethasone on expression patterns of markers of inflammatory activation of microglia/macrophages by immunohistochemistry. Endothelial-monocyte activating polypeptide II (EMAP-II), P2X4 receptor (P2X4R) and allograft-inflammatory factor-1 (AIF-1) were reported to be associated with the activation of microglia/macrophages post central nervous system (CNS) injury and may play roles in inflammatory cascades of secondary brain damage. Dexamethasone significantly suppressed the accumulation of EMAP-II(+), P2X4R(+) or AIF(+) cells at Day-1 and 2 post-brain-trauma but not on Days 4 and 6, which is in accordance with the reported short- but not long-term protective effects of dexamethasone in TBI. These findings indicate a rather rapid but transient anti-inflammatory effect of dexamethasone in TBI.
authors.affiliation: Institute of Brain Research, University of Tübingen, Calwer Str. 3, 72076 Tübingen, Germany. zhangzy@gmx.de
authors.forename: Zhiyuan
authors.initials: Z
authors.lastname: Zhang
authors.forename: Zhiren
authors.initials: Z
authors.lastname: Zhang
authors.forename: Matthias
authors.initials: M
authors.lastname: Artelt
authors.forename: Michael
authors.initials: M
authors.lastname: Burnet
authors.forename: Hermann J
authors.initials: HJ
authors.lastname: Schluesener
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology*; D002135:Calcium-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D003907:Dexamethasone / Q000494:pharmacology*; D007150:Immunohistochemistry; D008262:Macrophage Activation / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D008840:Microfilament Proteins; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics; D016601:RNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D011917:Rats, Inbred Lew; D018048:Receptors, Purinergic P2 / Q000096:biosynthesis / Q000235:genetics; D058848:Receptors, Purinergic P2X4
chemical_list: C100745:Aif1 protein, rat; D000893:Anti-Inflammatory Agents; D002135:Calcium-Binding Proteins; D016207:Cytokines; D008840:Microfilament Proteins; D009363:Neoplasm Proteins; C548226:P2RX4 protein, human; C548228:P2rx4 protein, rat; D016601:RNA-Binding Proteins; D018048:Receptors, Purinergic P2; D058848:Receptors, Purinergic P2X4; C077219:small inducible cytokine subfamily E, member 1; D003907:Dexamethasone