Abstract
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.
Highlights
Increased inflammatory reaction is elicited after traumatic brain injury (TBI) in areas proximal and distal to the locus of primary insult [1,2,3]
A cohort of 72 animals was divided into 6 experimental groups in a randomized fashion (n = 12 per group): control group (C), intact rats; control hyperbaric oxygenation (HBO) group (CHBO), intact rats subjected to the HBO protocol for 10 consecutive days; sham group (S), the animals that underwent surgical procedure without skull opening and were sacrificed 10 days after injury; sham HBO group (SHBO), the animals that underwent sham surgery and were subjected to the HBO protocol for 10 consecutive days; lesion group (L), the animals that passed cortical stab injury (CSI) and were sacrificed at 10th dpi; and lesion HBO group (LHBO), CSI rats subjected to the HBO protocol for 10 consecutive days
It is important to note that there was no statistically significant difference between data obtained for C, CHBO, S, and SHBO groups and, for immunohistochemical analysis all comparisons were done with respect to intact controls
Summary
Increased inflammatory reaction is elicited after traumatic brain injury (TBI) in areas proximal and distal to the locus of primary insult [1,2,3]. An invasion of macrophages and neutrophils into the impact area is triggered, and they initiate much of the inflammation and swelling in damaged areas that can directly affect the outcome after TBI [4, 5]. It is well documented that the basic mechanisms underlying neuroinflammatory cascade involves activation and ligation of CD40 ligand (CD40L, termed CD154, or GP39) and its counter receptor CD40 [6]. On the surface of vascular endothelial cells, CD40/CD40L ligation upregulates production of ICAM-1 (CD54), an adhesion molecule that is important for transendothelial migration of neutrophils and propagation of inflammation [7, 8]. Considering that CD40/CD40L dyad fosters neuroinflammation, some studies suggest that CD40/CD40L interaction may be involved in modulating the outcome from injuries of the brain [9,10,11]. Strategies aimed at suppressing CD40/CD40L/ICAM1 expression, may attenuate inflammation and neuronal damage after TBI, which will be of benefit in recovery [12]
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