Na+-dependent chloride transporter (NKCC1)-null mice exhibit less gray and white matter damage after focal cerebral ischemia
Na+-dependent chloride transporter (NKCC1)-null mice exhibit less gray and white matter damage after focal cerebral ischemia
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DOI：
10.1038/sj.jcbfm.9600006
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发表时间：
2005-01-01
影响因子：
6.3
通讯作者：
Sun, DD
中科院分区：
文献类型：
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作者：
Chen, H;Luo, J;Sun, DD
我们先前在体内和体外缺血模型中证明了抑制Na+-K+-Cl-共转运体1(NKCC1)的药理作用具有神经保护作用。在这项研究中，我们研究了基因消融NKCC1是否提供了缺血后的神经保护。结扎左侧大脑中动脉(MCAO)2小时后再灌流10或24小时，造成局灶性脑缺血模型。在NKCC1野生型(NKCC1(+/+))小鼠中，大脑中动脉闭塞2小时，再灌注10或24小时可导致脑梗塞(类似于85 mm(3))。NKCC1(-/-)小鼠的脑梗塞体积减少了30%到46%。杂合突变(NKCC1(+/-))小鼠的心肌梗死发生率降低了28%(P>；0.05)。NKCC1(+/+)小鼠大脑中动脉闭塞2小时、再灌注24小时，脑水肿程度明显增加。相比之下，NKCC1(+/-)和NKCC1(-/-)小鼠的水肿量减少了50%(P
We previously demonstrated that pharmacological inhibition of Na+-K+-Cl- cotransporter isoform 1 (NKCC1) is neuroprotective in in vivo and in vitro ischemic models. In this study, we investigated whether genetic ablation of NKCC1 provides neuroprotection after ischemia. Focal ischemia was induced by 2 hours occlusion of the left middle cerebral artery (MCAO) followed by 10 or 24 hours reperfusion. Two hours MCAO and ten or twenty-four hours reperfusion caused infarction (similar to85 mm(3)) in NKCC1 wild-type (NKCC1(+/+)) mice. Infarction volume in NKCC1(-/-) mice was reduced by similar to30% to 46%. Heterozygous mutant (NKCC1(+/-)) mice showed similar to28% reduction in infarction (P>0.05). Two hours MCAO and twenty-four hours reperfusion led to a significant increase in brain edema in NKCC1(+/+) mice. In contrast, NKCC1(+/-) and NKCC1(-/-) mice exhibited similar to50% less edema (P