Tan Kian H, Purcell Wendy M, Heales Simon J R, McLeod Julie D, Hurst Roger D
Department of Neurochemistry, Institute of Neurology, Univeristy College London, London WC1N 3BG, UK.
Neuroreport. 2002 Dec 20;13(18):2593-7. doi: 10.1097/00001756-200212200-00042.
In this study we evaluated the role of the multi-drug transporter p-glycoprotein (Pgp) in the process of activated T lymphocyte-mediated blood-brain barrier dysfunction as described previously. Lymphocyte exposure induced significant endothelial cell death and there was an elevation of the expression of Pgp in the surviving cells. Inhibition of Pgp function using the antibody MRK16 and verapamil displayed a dose-dependent prevention of T cell mediated endothelial cell death and barrier breakdown. These data suggest that the activity of Pgp at the blood-brain barrier may play a role in lymphocyte induced barrier cell damage and a role as a possible survival mechanism to prevent further endothelial cell death in later stages of inflammation.
在本研究中，我们如先前所述评估了多药转运体P-糖蛋白（Pgp）在活化的T淋巴细胞介导的血脑屏障功能障碍过程中的作用。淋巴细胞暴露诱导了显著的内皮细胞死亡，并且存活细胞中Pgp的表达有所升高。使用抗体MRK16和维拉帕米抑制Pgp功能显示出对T细胞介导的内皮细胞死亡和屏障破坏具有剂量依赖性的预防作用。这些数据表明，Pgp在血脑屏障处的活性可能在淋巴细胞诱导的屏障细胞损伤中起作用，并且在炎症后期作为一种可能的存活机制，以防止内皮细胞进一步死亡。
