拟缺血性损伤对rBMECs上Pgp的影响和其机制研究.pdf

摘要 BrainMicrovascular 目的：探讨拟缺血性损伤对大鼠脑微血管内皮细胞(Rat Endothelial necrosis 在共培养体系内室加入肿瘤坏死因子(Tumor (Nitric．oxide C，PKC)的抑制剂H398、 synthase，NOS)、蛋白激酶C(Proteinkinase Permeability Rhl23的表观渗透系数(Apparent Sodim 对rBMECs上P．gP功能的变化；测定荧光素钠(Fluorescein Blot法确定可能引起 室到外室的Papp监测rBMECs紧密连结的完整性；采用Western P—gp表达和功能变化的因子、加入相应的抑制剂测定各因子和P—gp表达变化的情况， 研究拟缺血性损伤对rBMECs上P．gp影响的机制。 影响。3．Western 表达；BIM对TNF一0【、NOS的表达无明显影响但可下调P—gP的表达。 特异性靶点。 关键词：P-gp，rBMECs，TNF氓NOS，PKC ABSTRACT theeffect inrBMECsunderischemic obiective：ToinvestigateofP—gP injury． BBB the culturesofrBMECs、neuron constructmodels Methods：Prepareprimary cells、astrocytea_nd invitrowithtranswell．2mMwasusedtoinducetherBMECsfor4h．Aftertreatmentwith Na2S204 in ofRhl23weremeasuredtoevaluate Na2S204rBMECs，the Papp paracellulartransportreflecting functionandthe ofNaFweremeasuredtoevaluatethe ofBBBmodels．Thecocultureof Papp quality rBMECs、neuron wasestablishedto the necrosis cells、astrocytes investigateP-gp、tumour 、nitricoMde kinaseC intherBMECsunderinduced synthase(NOS)、protein6KC)expression by Westernblot．Theinfluenceof tools on Na2S204using pharmacologicalincludingH398，L-NMMA，BIM the aswellasRhl23transendothelialtransfer． P-gpexpression Results：1．Thecocultureof