Protection against ischemic brain damage in rats by immunophilin ligand GPI-1046
Protection against ischemic brain damage in rats by immunophilin ligand GPI-1046
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DOI：
10.1002/jnr.20067
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发表时间：
2004-05-01
影响因子：
4.2
通讯作者：
Abe, K
中科院分区：
文献类型：
--
作者：
Li, F;Omori, N;Abe, K
为探讨亲免疫蛋白配体GPI-1 046对缺血性脑损伤的影响，采用大鼠脑短暂性大脑中动脉闭塞（MCAO） 90 min。与载药治疗相比，GPI-1046在24小时再灌注时可显著减少梗死面积，抑制轮状酶活性。GPI-1046治疗后，脑内FKBP12、FKBP52、caspase-8、细胞色素c和caspase-3阳性的免疫反应性和细胞数量也显著降低。提示GPI-1046通过抑制缺血区轮状酶活性和FKBP12-、FKBP52-、caspase-8-、细胞色素c-、caspase-3阳性细胞数量的增加，显著降低脑缺血大鼠梗死面积，并对脑缺血大鼠起到神经保护作用。(C) 2004 Wiley-Liss, Inc。
To determine the effect of immunophilin ligand GPI-1 046 on ischemic brain injury, 90 min of transient middle cerebral artery occlusion (MCAO) was carried out in rat brains. In contrast to cases treated with vehicle, the infarct volume was reduced greatly and rotamase activity was inhibited significantly at 24 hr of reperfusion by treatment with GPI-1046. Immunoreactivity and the number of cells stained positively for FKBP12, FKBP52, caspase-8, cytochrome c, and caspase-3 were also reduced markedly in the brain after GPI-1046 treatment. The present results suggest that GPI-1046 significantly decreased infarct volume and provided neuroprotective effect on rats after transient focal cerebral ischemia by inhibiting the increase of rotamase activity and of the number of FKBP12-, FKBP52-, caspase-8-, cytochrome c-, and caspase-3-positive cells in the ischemic area. (C) 2004 Wiley-Liss, Inc.