论文部分内容阅读
葡萄糖通过血脑屏障从血液中进入脑组织必须依赖葡萄糖转运蛋白(glucose transporter,GLUT)的帮助.GLUT1是血脑屏障上最主要的GLUT,也是脑毛细血管壁内皮细胞的分子标记.动物研究显示在急性脑缺血后脑内的GLUT1表达增加.检测了7例慢性微血管缺血性脑血管病变(ischemic cerebrovascular diseases,ICVD)的尸检脑组织中的GLUT1水平,并与11例同龄对照组比较.结果发现GLUT1水平在ICVD组中降低.其降低可能是由于低氧诱导因子-1α(hypoxia-induciblefactor-1α,HIF-1α)的下调所致.但是,在ICVD脑组织中的GLUT1水平降低不伴随有蛋白质O-GlcNAc糖基化水平的下降.上述结果为探讨脑缺血病变的机理提供了新线索.
Glucose entering the brain from the bloodstream through the blood-brain barrier must rely on the help of glucose transporter (GLUT1), the most prominent GLUT on the blood-brain barrier and a molecular marker of endothelial cells in the brain capillary walls. The expression of GLUT1 in the brain increased after acute cerebral ischemia.The GLUT1 levels in the autopsy brain tissue of 7 patients with chronic microvascular ischemic cerebrovascular disease (ICVD) were detected and compared with 11 control subjects of same age The level of GLUT1 was found to decrease in ICVD group, which may be attributed to the down-regulation of hypoxia-inducible factor-1α (HIF-1α), however, the decrease of GLUT1 level in ICVD brain tissues was not accompanied by Protein O-GlcNAc glycosylation levels decline.The above results provide a new clues to explore the mechanism of cerebral ischemia.