rhorock信号通路介导缺氧所致人肺微血管内皮细胞肌动蛋白细胞骨架重构和重组人白介素10对缺氧条件下人肺微血管内皮细胞凋亡变化规律的影响.docx

《rhorock信号通路介导缺氧所致人肺微血管内皮细胞肌动蛋白细胞骨架重构和重组人白介素10对缺氧条件下人肺微血管内皮细胞凋亡变化规律的影响.docx》由会员分享，可在线阅读，更多相关《rhorock信号通路介导缺氧所致人肺微血管内皮细胞肌动蛋白细胞骨架重构和重组人白介素10对缺氧条件下人肺微血管内皮细胞凋亡变化规律的影响.docx（2页珍藏版）》请在第壹文秘上搜索。

1、rhorock信号通路介导缺氧所致人肺微血管内皮细胞肌动蛋白细胞骨架重构和重组人白介素10对缺氧条件下人肺微血管内皮细胞凋亡改变规律的影响广州医学院硕士学位论文5Hypoxia-InducedReorganizationofActinCytoskeletonMediatedbyRho-ROCKSignalPathwayinHumanPulmonaryMicrovascularEndothelialCellsandTheEffectofRecombinationHumanInterleukin10onHypoxia-inducedApoptosisinHumanPu1nonaryMicrovas

2、cularEndothelialCellsProf.Qi-IiangCuiCandidate:JingMoSupervisor:Abstract1Objective1.1ToinvestigatetheroleofRho-ROCKsignalpathwayinthereorganizationofactincytoskeletonandthechangesofmorphologyinducedbyhypoxiainhumanpulmonarymicrovascularendothelialcelIs(HPMVECs).1.2Toinvestigatetheameliorativemechani

3、smofrecombinatinghumaninterleukin10(rhI1.-10)throughinhibitingtheapoptosisandCaSPaSe-3activityinhypoxia-inducedhumanpulmonarymicrovascularendothelialcelIs.2MaterialsandMethods2.1Duringtheexperimentsthehumanpulmonarymicrovascularendothelialcellswereexposedtohypoxiafor6h,12hand24hrespectivelyorpre-inc

4、ubatedwithaspecialinhibitorofKOCK,H-1152(10nmol1.)for0.5hbeforehypoxiainvitro.ThereorganizationofcellularactincytoskeletonandthechangesofcellularmorphologyinducedbyhypoxiaorpretreatmentofHl152wereexaminedbylaserscanningconfocal广州医学院硕士学位论文6microscopy(1.SCM).TheF-actinmeanfluorescenceintensityofeachgr

5、oupwasexaminedbyflowcytometric.2.2TheculturedHPMVECswererandomizedtonormalcontrolgroup,hypoxiacontrolgroup,thelow-rhI1.-10interventiongroup,middle-rhI1.-10interventiongroupandhigh-doserhI1.-10interventiongroup.Thenormalgroupwasculturedwiththe37eCand5%CO2condition,andthehypoxiagroupswereculturedwith5%CO2,95%N2condition.Theculturedtimelastedfor4h,12h,24hand48hrespectively.Therelativecaspase-3activityofal1groupsweredetectedwithChromatometryattheendof4h,12h,24hand48h.Theapoptosisfluorescenceintensitywereanalyzedbythefluorescentmicroscopeattheendof24hwithstatisticalmet.