脑络欣通通过激活HIF-1α/VEGF信号通路促进氧糖剥夺/复氧 复糖损伤后大鼠的脑微血管内皮细胞增殖

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Abstract：ObjectiveToinvestigatetheefectsofNaoluoXintongDecoction（NLXTD）onproliferationofratbrainmicrovascular endothelial cels （BMECs）afteroxygen-glucose deprivation/reoxygenation （OGD/R）injuryandroleof theHIF-1α/VEGF pathway in mediating its effect.Methods Usinga BMEC model of OGD/R，we tested the effects of 10% NLXTD-medicated rat serum，alone orin combination with 2ME2 or 10% NAKL，on cell proliferation，migration，tube-forming ability and permeabilitysngCCK-8ssayansellaberssayubeomatioassadpemeabilitysy.Cellularo of VEGFandNotchweredetectedusingELISandlaserconfocalimmunofluorescenceanalsisandteexpressionsofHF1αVEGFR2，Notch1，RKandP-RK1/2protesweredetectedithWestenbloing.ResultsOGD/Rinjuryigcantly decreasedviabilityof BMECs.NLXTD treatmentof thecells with OGD/R couldsignificantly promotedcell proliferation， migrationandtubeformationabilitybuttheseeffcts werestronglyatenuatedbyapplicationof2ME2.NLXTDtreatmentalso significantlyincreasedthepercentagesof VEGF-andNotch-positivecelsinthecellmodelsandobviouslyenhancedthe expresionlelsof-otcd1/.uiooteraiati formation of rat BMECs after OGD/R injury possibly by activating the HIF-1α/VEGF signaling pathway.

Keywords：ischemicstroke;NaoluoXintongDecoction;HIF-1α/VEGFsignalingpathway;oxygen-glucosedeprivation/ reoxygenation injury;cerebral microvascular endothelial cells

缺血性脑卒中是由于缺血、缺氧等因素导致脑部血液循环障碍，进而引发脑组织缺血性坏死或软化的一类疾病。（剩余14378字）