硒对体外培养人甲状腺细胞氧化损伤、凋亡及超微结构的影响-内分泌与代谢病专业论文.docx

Theeffectofseleniumonoxidativedamage，apoptosisandultrastructureofhumanthyrocytecultureinvitroAbstractObjectiveToinvestigatetheinfluenceofselenium(Se)onoxidativedamage，apoptosisandultrastructureofhumanthyrocyteinducedbyH202cultureinvitro．MethodsThehumanthyroidepitheliumcells(TEC)frompara—adenomanormaltissuesofpatientswiththyroidadenomawerecultured．AddeddifferentconcentrationH202(O～800／Mmol／L)intothyrocyteofmonolayercultureafterwithorwithoutSe(10。mmol／L)．ThethyrocyteviabilitywasdetectedusingMTTstain．Flowcytometrydetectedapoptosisratesofthyrocyte．TheactivityofGSH-PxandcontentofMDAweredetemined．Andthethyrocyteultramicrostructureofeachgroupwereobserved．ResultsWhenthethyrocyteexposedtoH202for24houfs，thecellviabilitydeclined，andcellapoptosisratesincreased，theGSH-Pxactivitydeclined，andMDAcontentincreased，witharelationofdose—effectresponseontherangof100-800／zmol／L．UndertheTEM，simplyseleniuminterventiongroupthyrocytesultrastructuresimilartothenormalcontrolgroup．WhenH202concentratmnwasl00--+200pmol／I．TEMshowedthatthyrocytesshoweddamagingchanges．WhenH202concentrationwas400～800pmol／L,TEMshowedthatthyrocytesshowedapoptosiseven death。AddingSe(10‘’mmol／L)intocell culturecouldeffectivelyincreaseviabilityandreducethethyrocyteapoptosiscausedbyH202．ComparedtothesimpleH202interventiongrouptheGSH-Pxactivitydeclined，andMDAcontentincreased．Seleniumpre-interventionineachgroupcanbeseencellultrastructureinjurylessensignificantly．ConclusionsH202caninhibitthe proliferationandinduceoxidativedamageevenapoptosisoftheTEC．SeleniumcouldprotectthyroidfollicularepithelialcellagainstoxidativedamagecausedbyH202．SeleniumcouldprotectthyroidfollicularepithelialcellagainstoxidativedamageandapoptosiscausedbyH202．Seleniummaybethatrolebyincreasing cellGSH·Pxactivityand toreducethecontentofMDAantagonistictheoxidativestresswaystoachieve．KeyWords：selenium；thyroid；oxidativedamage；apoptosis；ultrastructure攻读学位论文期间的研究成果学位论文独创性声明本人声明，所呈交的学位论文系本人在导师指导下独立完成的研究成果。文中依法引用他人的成果，均已做出明确标注或得到许可。论文内容未包含法律意义上已属于他人的任何形式的研究成果，也不包含本