Inhibition of MEK/ERK 1/2 pathway reduces pro-inflammatory cytokine interleukin-1 expression in focal cerebral ischemia
Inhibition of MEK/ERK 1/2 pathway reduces pro-inflammatory cytokine interleukin-1 expression in focal cerebral ischemia
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DOI：
10.1016/j.brainres.2003.09.074
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发表时间：
2004-01-16
期刊：
影响因子：
2.9
通讯作者：
Yang, GY
中科院分区：
文献类型：
--
作者：
Wang, ZQ;Wu, DC;Yang, GY
有研究提出，丝裂原活化蛋白激酶（MAPK）途径可能在脑缺血过程中调节促炎细胞因子，如介素-1。我们之前的研究表明，细胞外信号调节激酶1和2 （ERK 1/2）在小鼠局灶性脑缺血时被激活[J]。Cereb。中华血液学杂志，2000,20(3):349 - 349。然而，erk1 /2在局灶性脑缺血中的作用尚不清楚。在这项研究中，我们报道了大脑中动脉闭塞（MCAO） 30分钟后，小鼠大脑缺血核心和焦周区域磷酸化- erk1 /2的体内表达增加。Western blot和免疫组化分析显示，1,4-二氨基-2,3-二氰-1,4-二丁二烯（U0126）对大鼠肝细胞凋亡有促进作用[J]。医学杂志。Chem. 273(1998) 18623]可以显著抑制MCAO 1-2小时后小鼠脑磷酸化- mek 1/2和磷酸化- erk 1/2的表达(p
It has been proposed that mitogen-activated protein kinase (MAPK) pathways may play a role in the regulation of pro-inflammatory cytokines, such as interlukine-1, during cerebral ischemia. Our previous study showed that extracellular-signal-regulated kinases 1 and 2 (ERK 1/2) were activated during focal cerebral ischemia in mice [J. Cereb. Blood Flow Metab. 20 (2000) 1320]. However, the effect of ERK 1/2 activation in focal cerebral ischemia is still unclear. In this study we reported that in vivo phospho-ERK 1/2 expression increased following 30 min of middle cerebral artery occlusion (MCAO) in the mouse brain in both the ischemic core and perifocal regions. Western blot analysis and immunohistochemistry demonstrated that pro-treatment with 1,4-diamino-2,3-dicyano-1,4-bis butadiene (U0126) [J. Biol. Chem. 273 (1998) 18623] could significantly inhibit mouse brain phospho-MEK 1/2 and phospho-ERK 1/2 expression after 1-2 h of MCAO (p