ROLES OF INFLAMMATION RESPONSE IN MICROGLIA CELL THROUGH TOLL-LIKE RECEPTORS 2/INTERLEUKIN-23/INTERLEUKIN-17 PATHWAY IN CEREBRAL ISCHEMIA/REPERFUSION INJURY

被引：82
作者：
Lv, M. [1 ,2 ]
Liu, Y. [3 ]
Zhang, J. [1 ,2 ]
Sun, L. [4 ]
Liu, Z. [1 ]
Zhang, S. [1 ]
Wang, B. [1 ]
Su, D. [2 ]
Su, Z. [1 ]
机构：
[1] Harbin Med Univ, Affiliated Hosp 1, Dept Neurol, Harbin 150001, Heilongjiang Pr, Peoples R China
[2] Harbin Med Univ, Affiliated Hosp 4, Dept Neurol, Harbin 150001, Heilongjiang Pr, Peoples R China
[3] Harbin Med Univ, Affiliated Hosp 1, Dept Neurosurg, Harbin 150001, Heilongjiang Pr, Peoples R China
[4] Harbin Med Univ, Dept Pharmacol, Harbin 150001, Heilongjiang Pr, Peoples R China
来源：
NEUROSCIENCE | 2011年 / 176卷
关键词：
cerebral ischemia reperfusion injury; microglia; Toll-like receptors; neuroinflammation; cytokines; FOCAL ISCHEMIA; EXPRESSION; ACTIVATION; LIPOPOLYSACCHARIDE; NEURODEGENERATION; CYTOKINE; IMMUNE; IL-23; IL-17; NEUROINFLAMMATION;
D O I：
10.1016/j.neuroscience.2010.11.066
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Microglial activation is one of the causative factors of neuroinflammation in cerebral ischemia. Activation via Toll-like receptors (TLRs) causes increased proinflammatory cytokine expression, such as interleukin-23 (IL-23) and interleukin-17 (IL-17), leading to inflammatory immune responses and neuronal damage. In this study, using a rat focal cerebral ischemia reperfusion (IR) model and an in vitro oxygen-glucose deprivation reperfusion (OGDR) system, we found that TLR2, IL-23 and IL-17 form an axis that leads to increased neuronal apoptosis. TLR2 activation results in IL-23 production which stimulates IL-17 production by microglia. This microglial axis may be a potential therapeutic target to control neuroinflammation in brain IR. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码：162 / 172
页数：11
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