β-ngf对过氧化氢损伤血管内皮细胞保护作用word论文.docxVIP

达，进而抑制H2O2 诱导HUVECs 损伤后的细胞凋亡，减轻H2O2 对HUVECs 细胞的损伤，从而对血管内皮细胞损伤发挥保护作用。通过本研究对于揭示神经生长因子因素与血管内皮细胞抵抗氧化损伤的关系具有重要意义，并对临床利用β- NGF防治动脉粥样硬化等心血管疾病具有重要参考价值。关键词：β-神经生长因子过氧化氢血管内皮细胞细胞凋亡氧化损伤AbstractObjective：Humanumbilicalveinendothelialcells (HUVECs)wereastheresearch object, thehydrogenperoxide(H2O2)wasused to construct the injury model induced bytheoxidativedamage,andthenstudytheprotectiveeffects of beta-NGF on vascularendothelial cellsand its mechanism.Methods：TheHUVECswassubculturedinvitroandthecellinjurymodelwasestablishedafterH2O2-induced.Thelowandhighdifferentconcentrationsof1,10,100?Mβ-NGFwereusedtotreattheoxidativeinjuryHUVECscellfor24h,whilesettingthe unjurycontrolgroupandthePBScontrolgroupaftertheH2O2injury.MTTmethodwas usedtodeterminethechangeofHUVECscellviability.Theapoptosisrateandreactive oxygen(ROS)ofHUVECswereanalyzedbyflowcytometry.Thecontentchangesof malondialdehyde(MDA),superoxidedismutase(SOD),glutathione(GSH)contentwere observedinHUVECs.Theendothelin-1(ET-1)andnitricoxide(NO)secretioncontent changeweretestedbyELISAmethod.TheexpressionchangeofTyrosinereceptorKinase A(TrkA),p75neurotrophinreceptor(p75NTR),apoptosis-relatedproteincaspase-3were detected bywestern-blot.Results ：After H2O2 induced HUVECs oxidative injury, compared with unjurycontrolgroup,inthePBScontrolgroupwhichinjuryafterH2O2oxidativedamage,the HUVECscellviabilitywasreducedsignificantly,P?0.05;andtheapoptosisrateandROS levelwereincreasedsignificantly,P?0.05;theMDAcontentwasincreasedsignificantly, whileSODandGSHactivityreducedsignificantly,P?0.05;theET-1secretioncontent was increased andNOsecretion was significantlydecreased,andP?0.05.comparedwiththePBScontrolgroup,1,10,100?Mβ-NGFtreatedgroupincreased theHUVECsviabilitysignificantly,P?0.05;andHUVECsapoptosisrateandROSlevel weresignificantlydecreased,P?0.05;thecontentofMDAweresignificantlydecreased, andmeantimetheactivityofSODandGSHwereincreased,showedstatisticalsignificance,P﹤0.05.ET-1secretioncontentweregraduallydecreasedandNOsecretioncontentw