简介：InordertoinvestigatewhetherlipoxinA4(LXA4)hasanantagonisticeffectonlipopolysaccharide(LPS)-inducedsynthesisofinterleukin(IL)-1β,IL-6andIL-8inratpulmonarymicrovascularendothelialcells(PMVEC),andtoexplorethemolecularmechanismsofsignalpathwayinLXA4actions,culturedPMVECweretreatedwithLPS,withorwithoutpreincubationwithLXA4.ProteinsofIL-1β,IL-6andIL-8insupernatantwereanalyzedbyenzyme-linkedimmunosorbentassay(ELISA).ExpressionsofmRNAofIL-1β,IL-6andIL-8weredeterminedbyRT-PCR.Expressionsofphosphorylationofphosphoinositide3-kinase(PI3-K)andmyeloiddifferentiationfactor88(MyD88)wereanalyzedbyWesternblot.ActivitiesofDNA-bindingofnuclearfactor-kappaB(NF-κB)andactivatorprotein-1(AP-1)weremeasuredbyelectrophoreticmobilityshiftassay(EMSA).TheresultsshowedthatLPSinducedproductionofIL-1β,IL-6andIL-8inratPMVECviaMyD88/PI3-K/NF-κBandAP-1pathway-dependentsignaltransduction.LPS-stimulatedexpressionofPI3-K,activitiesofNFκBandAP-1,secretionofproteinandexpressionofmRNAofIL-1β,IL-6andIL-8butnotMyD88expressioninPMVECwereinhibitedbyLXA4inadose-dependentmanner.Inconclusion,LXA4inhibitssynthesisofIL-1β,IL-6andIL-8bydown-regulationofPI3-K/NF-κBandAP-1signalpathwayinPMVEC.

简介：ThisstudywasaimedtoobservetheexpressionofP70S6kinase(P70S6K)inoralaciniccellcarcinoma.PT0S6kinaseexpressionwasexaminedbymeansofWestern-blottestandActivityas-say.Specimenswerefrom30casesoforalaciniccellcarcinomaand15casesofnormaloraltissuewereusedascontrols.StatisticalanalysissoftwareSPSS10.0wasusedforttesttodeterminetherelationshipbetweengeneexpressionandclinicalfeatures.TheexpressionlevelofP70S6Kincreasedobviouslyinoralaciniccellcarcinomatissue(P<0.01).ActivityassaywasthesameastheWestemblottest(P<0.01).P70S6Kexpressionlevelandactivityplayedanimportantroleinthedevelopmentoforalaciniccellcarcinoma.Inconclusion,P70S6Kisamplifiedandoverexpressedinoralaciniccellcarci-nomatissue,whichsuggestsapotentialoncogenicfunction.P70S6KandotherpossibletargetsofmTORcontributesignificantlytotumordevelopmentandthatinhibitionoftheseproteinsmaybethera-peuticforcancerpatients.OverexpressionofP70S6Kmaybeinvolvedinthepathogenesisoforalacin-iccellcarcinoma.

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简介：目的：基于PI3K/AKT通路探讨芪灵扶正清解颗粒对肝癌细胞凋亡的影响。方法：HepG2细胞培养条件见参考文献[2]。种板24h后，分为2组，其中空白组更换新鲜培养液培养；给药组以5mg/mL的含芪灵培养液处理，干预48h后继续后续实验。按照传统方法提取蛋白样本。结果：透射电镜结果显示与空白组相比，芪灵组细胞具备明显的早期凋亡特征，证实芪灵扶正清解颗粒能够诱导HepG2细胞凋亡。此外，本研究中芪灵组磷酸化的PI3K、AKT蛋白表达量较空白组显著下降，说明芪灵能够抑制肝癌细胞HepG2中PI3K/AKT通路的活性。结论：芪灵扶正清解颗粒促进肝癌细胞凋亡并抑制其增殖能力收可能与PI3K/AKT信号通路有关。

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