简介：Inthepresentstudy,theeffectsofPleurotusnebrodensispolysaccharide(PN-S)ontheimmunefunctionsofimmunosuppressedmiceweredetermined.Theimmunosuppressedmousemodelwasestablishedbytreatingthemicewithcyclophosphamide(40mg/kg/2d,CY)throughintraperitonealinjection.TheresultsshowedthatPN-SadministrationsignificantlyreversedtheCY-inducedweightloss,increasedthethymicandsplenicindices,andpromotedproliferationofTlymphocyte,Blymphocyte,andmacrophages.PN-SalsoenhancedtheactivityofnaturalkillercellsandincreasedtheimmunoglobulinM(IgM)andimmunoglobulinG(IgG)levelsintheserum.Inaddition,PN-Streatmentsignificantlyincreasedthephagocyticactivityofmouseperitonealmacrophages.PN-Salsoincreasedthelevelsofinterleukin-6(IL-6),tumornecrosisfactor-α(TNF-α),interferon-γ(INF-γ),andnitricoxide(NOS)insplenocytes.qRT-PCRresultsalsoindicatedthatPN-SincreasedthemRNAexpressionofIL-6,TNF-α,INF-γ,andnitricoxidesynthase(iNOS)inthesplenocytes.TheseresultssuggestthatPN-Streatmentenhancestheimmunefunctionofimmunosuppressedmice.Thisstudymayprovideabasisfortheapplicationofthisfungusinadjacentimmunopotentiatingtherapyagainstcancerandinthetreatmentofchemotherapy-inducedimmunosuppression.

简介：AnovelPleurotusnebrodensispolysaccharide(PN-S)waspurifiedandcharacterized,anditsimmune-stimulatingactivitywasevaluatedinRAW264.7macrophages.PN-SinducedtheproliferationofRAW264.7cellsinadose-dependentmanner,asdeterminedbytheMTTassay.AfterexposuretoPN-S,thephagocytosisofthemacrophageswassignificantlyimproved,withremarkablechangesinmorphologybeingobserved.FlowcytometricanalysisdemonstratedthatPN-SpromotedRAW264.7cellstoprogressthroughSandG2/Mphases.PN-Streatmentenhancedtheproductionsofinterleukin-6(IL-6),nitricoxide(NO),interferongamma(INF-γ),andtumornecrosisfactor-α(TNF-α)inthemacrophages,withup-regulationofmRNAexpressionsofinterleukin-6(IL-6),induciblenitricoxidesynthase(iNOS),interferongamma(INF-γ)andtumornecrosisfactor-α(TNF-α)beingobservedinadose-dependentmanner,asmeasuredbyqRT-PCR.Inconclusion,theseresultssuggestthatthepurifiedPN-Scanimproveimmunitybyactivatingmacrophages.

简介：目的：研究血竭素高氯酸盐（DracorhodinPerchlorate，DP）抗乳腺癌作用及作用机制。方法：四甲基噻唑蓝法分析60μmol·L^-1DP作用不同时间后，其对肿瘤细胞的抑制率；细胞形态学分析、细胞核形态学分析和DNA片段化分析确定细胞凋亡的发生；Rhodamine123染色分析细胞线粒体膜电位；Western检测细胞凋亡相关特别是线粒体相关蛋白表达。结果：60μmol·L^-1DP时间依赖性地抑制人乳腺癌MCF-7细胞生长；DP抑制细胞生长通过诱导MCF-7细胞凋亡来实现；DP诱导细胞凋亡时，其活化了线粒体通路蛋白caspase-9，剪切了DNA损伤修复蛋白PARP；进一步研究发现DP诱导细胞凋亡的主要原因是其降低了细胞线粒体膜电位（正常膜电位细胞百分比93．11％；DP处理后正常膜电位细胞百分比37．45％）；而线粒体上Bcl-2、Bcl—XL表达减少，Bax、Bak增多是DP改变线粒体膜电位的主要原因。结论：DP通过调节线粒体通路来促进细胞凋亡。