Delayed brain ischemia tolerance induced by electroacupuncture pretreatment is mediated via MCP-induced protein 1.
Delayed brain ischemia tolerance induced by electroacupuncture pretreatment is mediated via MCP-induced protein 1.
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DOI：
10.1186/1742-2094-10-63
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发表时间：
2013-05-10
影响因子：
9.3
通讯作者：
Kolattukudy PE
中科院分区：
文献类型：
--
作者：
Jin Z;Liang J;Wang J;Kolattukudy PE
近年来的研究表明，电针预处理可诱导大鼠局灶性脑缺血耐受。本研究旨在确定单核细胞趋化蛋白诱导的蛋白1（MCPIP 1），最近发现的新的炎症反应的调节剂，在局灶性脑缺血动物模型中的EA预处理所赋予的脑神经保护的参与，并阐明EA预处理诱导缺血脑耐受的机制。最后一次EA预处理结束后24小时，雄性C57 BL/6小鼠和MCPIP 1基因敲除小鼠通过大脑中动脉阻塞（MCAO）90分钟诱导局灶性脑缺血。采用qRT-PCR、Western blot和免疫组织化学方法检测MCPIP 1基因的转录和表达。观察缺血/再灌注后大鼠神经行为学评分、脑梗死体积、脑组织炎症因子、白细胞浸润及NF-κB信号的变化。电针预处理小鼠脑MCPIP 1蛋白和mRNA水平显著升高。与非电针组相比，电针预处理显著减轻了MCAO后野生型小鼠脑中的梗死体积、神经功能缺损、促炎细胞因子的上调和白细胞浸润。MCPIP 1基因敲除小鼠与对照组相比，电针预处理诱导的耐受性不明显。此外，与非EA对照组相比，EA预处理的野生型小鼠MCAO后NF-κB信号的活化显著降低，并且MCPIP 1缺陷小鼠不能赋予EA预处理诱导的MCAO后NF-κB信号抑制。我们的数据表明，MCPIP 1缺陷导致显着缺乏EA预处理诱导的脑保护作用后MCAO与对照组相比，MCPIP 1参与EA预处理诱导的延迟性脑缺血耐受。
Emerging studies have demonstrated that pretreatment with electroacupuncture (EA) induces significant tolerance to focal cerebral ischemia. The present study seeks to determine the involvement of monocyte chemotactic protein-induced protein 1 (MCPIP1), a recently identified novel modulator of inflammatory reactions, in the cerebral neuroprotection conferred by EA pretreatment in the animal model of focal cerebral ischemia and to elucidate the mechanisms of EA pretreatment-induced ischemic brain tolerance. Twenty-four hours after the end of the last EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 minutes in male C57BL/6 mice and MCPIP1 knockout mice. Transcription and expression of MCPIP1 gene was monitored by qRT-PCR, Western blot and immunohistochemistry. The neurobehavioral scores, infarction volumes, proinflammatory cytokines and leukocyte infiltration in brain and NF-κB signaling were evaluated after ischemia/reperfusion. MCPIP1 protein and mRNA levels significantly increased specifically in mouse brain undergoing EA pretreatment. EA pretreatment significantly attenuated the infarct volume, neurological deficits, upregulation of proinflammatory cytokines and leukocyte infiltration in the brain of wild-type mice after MCAO compared with that of the non-EA group. MCPIP1-deficient mice failed to evoke EA pretreatment-induced tolerance compared with that of the control MCPIP1 knockout group without EA treatment. Furthermore, the activation of NF-κB signaling was significantly reduced in EA-pretreated wild-type mice after MCAO compared to that of the non-EA control group and MCPIP1-deficient mice failed to confer the EA pretreatment-induced inhibition of NF-κB signaling after MCAO. Our data demonstrated that MCPIP1 deficiency caused significant lack of EA pretreatment-induced cerebral protective effects after MCAO compared with the control group and that MCPIP1 is involved in EA pretreatment-induced delayed brain ischemia tolerance.
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DOI：
10.1084/jem.20092641
发表时间：
2010-12-20
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Liang J;Saad Y;Lei T;Wang J;Qi D;Yang Q;Kolattukudy PE;Fu M
通讯作者：
Fu M
影响因子：
1.6
作者：
Gu, G.;Zhang, Z.;Li, W.
通讯作者：
Li, W.
重复电针预处理减弱大鼠局灶性脑缺血后基质金属蛋白酶9的表达和活性
影响因子：
1.9
作者：
Dong, Hui;Fan, Yan-Hong;Xiong, Li-Ze
通讯作者：
Xiong, Li-Ze
影响因子：
82.9
作者：
Liesz, Arthur;Suri-Payer, Elisabeth;Veltkamp, Roland
通讯作者：
Veltkamp, Roland
ERK 1/2 激活参与大鼠大麻素 CB1 受体电针预处理
影响因子：
2.9
作者：
Du, Juan;Wang, Qiang;Chen, Shaoyang
通讯作者：
Chen, Shaoyang