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Mediators of Inflammation
Volume 2015 (2015), Article ID 498405, 17 pages
Research Article

Repetitive Hyperbaric Oxygenation Attenuates Reactive Astrogliosis and Suppresses Expression of Inflammatory Mediators in the Rat Model of Brain Injury

1Department of Neurobiology, Institute for Biological Research “Sinisa Stankovic”, University of Belgrade, 11060 Belgrade, Serbia
2Institute of Medical Physiology “Richard Burian”, School of Medicine, University of Belgrade, 11000 Belgrade, Serbia
3Centre for Hyperbaric Medicine, 11040 Belgrade, Serbia
4Institute of Physiology and Biochemistry, Faculty of Biology, University of Belgrade, 11001 Belgrade, Serbia

Received 3 December 2014; Revised 5 February 2015; Accepted 8 March 2015

Academic Editor: Amos Douvdevani

Copyright © 2015 Irena Lavrnja et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The exact mechanisms by which treatment with hyperbaric oxygen (HBOT) exerts its beneficial effects on recovery after brain injury are still unrevealed. Therefore, in this study we investigated the influence of repetitive HBOT on the reactive astrogliosis and expression of mediators of inflammation after cortical stab injury (CSI). CSI was performed on male Wistar rats, divided into control, sham, and lesioned groups with appropriate HBO. The HBOT protocol was as follows: 10 minutes of slow compression, 2.5 atmospheres absolute (ATA) for 60 minutes, and 10 minutes of slow decompression, once a day for 10 consecutive days. Data obtained using real-time polymerase chain reaction, Western blot, and immunohistochemical and immunofluorescence analyses revealed that repetitive HBOT applied after the CSI attenuates reactive astrogliosis and glial scarring, and reduces expression of GFAP (glial fibrillary acidic protein), vimentin, and ICAM-1 (intercellular adhesion molecule-1) both at gene and tissue levels. In addition, HBOT prevents expression of CD40 and its ligand CD40L on microglia, neutrophils, cortical neurons, and reactive astrocytes. Accordingly, repetitive HBOT, by prevention of glial scarring and limiting of expression of inflammatory mediators, supports formation of more permissive environment for repair and regeneration.