INTERLEUKIN-10 MEDIATES THE NEUROPROTECTION OF HYPERBARIC OXYGEN THERAPY AGAINST TRAUMATIC BRAIN INJURY IN MICE

被引:76
作者
Chen, X. [1 ]
Duan, X. -S. [1 ]
Xu, L. -J. [1 ]
Zhao, J. -J. [2 ]
She, Z. -F. [1 ]
Chen, W. -W. [1 ]
Zheng, Z. -J. [1 ]
Jiang, G. -D. [1 ]
机构
[1] 113th Hosp PLA, Dept Hyperbar Oxygen, Ningbo 315040, Zhejiang, Peoples R China
[2] 305th Hosp PLA, Dept Neurol, Beijing, Peoples R China
关键词
interleukin-10; hyperbaric oxygen; traumatic brain injury; apoptosis; inflammation; edema; SPINAL-CORD-INJURY; NEURONAL APOPTOSIS; BARRIER FUNCTION; EDEMA; EXPRESSION; DAMAGE; MATRIX-METALLOPROTEINASE-9; NEUROINFLAMMATION; CASPASES; IMPACT;
D O I
10.1016/j.neuroscience.2013.11.036
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 1 h at 2.0 absolute atmosphere (ATA) in 100% O-2. 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-1 beta, 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. (C) 2014 Published by Elsevier Ltd. on behalf of IBRO.
引用
收藏
页码:235 / 243
页数:9
相关论文
共 35 条
[1]   Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model [J].
Acosta, Sandra A. ;
Tajiri, Naoki ;
Shinozuka, Kazutaka ;
Ishikawa, Hiroto ;
Grimmig, Bethany ;
Diamond, David ;
Sanberg, Paul R. ;
Bickford, Paula C. ;
Kaneko, Yuji ;
Borlongan, Cesar V. .
PLOS ONE, 2013, 8 (01)
[2]   Object recognition in rats and mice: a one-trial non-matching-to-sample learning task to study 'recognition memory' [J].
Bevins, Rick A. ;
Besheer, Joyce .
NATURE PROTOCOLS, 2006, 1 (03) :1306-1311
[3]   Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies [J].
Bramlett, Helen M. ;
Dietrich, W. Dalton .
NEUROTRAUMA: NEW INSIGHTS INTO PATHOLOGY AND TREATMENT, 2007, 161 :125-141
[4]   IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury:: relationship to IL-6, TNF-α, TGF-β1 and blood-brain barrier function [J].
Csuka, E ;
Morganti-Kossmann, MC ;
Lenzlinger, PM ;
Joller, H ;
Trentz, O ;
Kossmann, T .
JOURNAL OF NEUROIMMUNOLOGY, 1999, 101 (02) :211-221
[5]   Central nervous system expression of IL-10 inhibits autoimmune encephalomyelitis [J].
Cua, DJ ;
Hutchins, B ;
LaFace, DM ;
Stohlman, SA ;
Coffman, RL .
JOURNAL OF IMMUNOLOGY, 2001, 166 (01) :602-608
[6]   Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments [J].
Donkin, James J. ;
Vink, Robert .
CURRENT OPINION IN NEUROLOGY, 2010, 23 (03) :293-299
[7]   Sustained sensory/motor and cognitive deficits with neuronal apoptosis following controlled cortical impact brain injury in the mouse [J].
Fox, GB ;
Fan, L ;
Levasseur, RA ;
Faden, AI .
JOURNAL OF NEUROTRAUMA, 1998, 15 (08) :599-614
[8]   Neuroprotection by IL-10-producing MOG CD4+T cells following ischemic stroke [J].
Frenkel, D ;
Huang, ZH ;
Maron, R ;
Koldzic, DN ;
Moskowitz, MA ;
Weiner, HL .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 2005, 233 (1-2) :125-132
[9]   Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury [J].
Knoblach, SM ;
Faden, AI .
EXPERIMENTAL NEUROLOGY, 1998, 153 (01) :143-151
[10]   Multiple caspases are activated after traumatic brain injury: Evidence for involvement in functional outcome [J].
Knoblach, SM ;
Nikolaeva, M ;
Huang, XL ;
Fan, L ;
Krajewski, S ;
Reed, JC ;
Faden, AI .
JOURNAL OF NEUROTRAUMA, 2002, 19 (10) :1155-1170