The aim of present study was to elucidate the role of Interleukin-10 (IL-10) in the neuroprotection of hyperbaric oxygen (HBO) against traumatic brain injury (TBI) in mice. The TBI in mice was induced by controlled cortical impact (CCI). HBO was given for 1h at 2.0 absolute atmosphere (ATA) in 100% O2. HBO enhanced the serumal and cerebral IL-10 protein levels in both sham-operated and TBI mice. HBO therapy after TBI reduced lesion volume, attenuated cerebral edema, improved neurological status including motor and cognitive function, inhibited apoptosis evidenced by decreased ratio of cleaved caspase-3 (C3) to pro-C3 and Bax expression and increased bcl-2 expression, and attenuated inflammation marked by reduced expression of IL-1β, IL-6, macrophage inflammatory protein-2 (MIP-2), and monocyte chemoattractant protein-1 (MCP-1) and activity of matrix metalloproteinase-9 (MMP9). In addition, HBO after TBI improved the blood-brain barrier, and upregulated the expression of tight junction proteins including zonula occludens-1 (ZO-1) and claudin-5. IL-10 deficiency aggravated TBI-induced damage in the brain and abrogated the beneficial effects of HBO on neuroinflammation, apoptosis, and edema after TBI. IL-10 deficiency itself had no significant effect on brain water content and neurological status. In conclusion, IL-10 played an important role in the neuroprotection of HBO therapy against TBI in mice.
Keywords: apoptosis; edema; hyperbaric oxygen; inflammation; interleukin-10; traumatic brain injury.
Copyright © 2014. Published by Elsevier Ltd.