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Dexamethasone attenuates early expression of three molecules associated with microglia/macrophages activation following rat traumatic brain injury

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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.

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Correspondence to Zhiyuan Zhang.

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Zhiyuan Zhang and Zhiren Zhang have equally contributed to this work.

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Zhang, Z., Zhang, Z., Artelt, M. et al. Dexamethasone attenuates early expression of three molecules associated with microglia/macrophages activation following rat traumatic brain injury. Acta Neuropathol 113, 675–682 (2007). https://doi.org/10.1007/s00401-007-0195-8

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