Boado R J
Department of Medicine, UCLA School of Medicine 90024, USA.
Neurosci Lett. 1995 Sep 15;197(3):179-82. doi: 10.1016/0304-3940(95)11930-u.
The blood-brain barrier (BBB) GLUT1 glucose transporter gene expression is known to be regulated by putative brain trophic factors. Therefore, the present study investigated the effect of a brain-derived peptide rich preparation containing a neurotrophic factor-like action [Cerebrolysin (Cl), EBEWE, Austria]. In cultures of brain capillary endothelial cells, Cl induced a transient increase in the abundance of BBB-GLUT1 relative to actin measured by reverse transcription-polymerase chain reaction during the first 2 h of incubation, whereas a significant reduction in the GLUT1 transcript was observed at 20 and 48 h. In addition, Cl abolished the fall in GLUT1 levels induced by actinomycin D. The present data suggest that brain-derived factors in Cl are able to modulate the expression of the BBB-GLUT1 gene increasing the BBB-GLUT1 transcript stability.
血脑屏障(BBB)葡萄糖转运蛋白1(GLUT1)基因的表达已知受假定的脑营养因子调控。因此,本研究调查了一种含有神经营养因子样作用的脑源性肽丰富制剂[脑活素(Cl),奥地利依比威制药公司]的作用。在脑毛细血管内皮细胞培养物中,在孵育的前2小时,通过逆转录-聚合酶链反应测量,Cl相对于肌动蛋白诱导BBB-GLUT1丰度短暂增加,而在20小时和48小时观察到GLUT1转录本显著减少。此外,Cl消除了放线菌素D诱导的GLUT1水平下降。目前的数据表明,Cl中的脑源性因子能够调节BBB-GLUT1基因的表达,增加BBB-GLUT1转录本的稳定性。