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1、题目：蜂胶黄酮抗H2O2诱导PC12细胞凋亡机制的研究药学毕业设计（论文）摘要目的观察蜂胶黄酮对过氧化氢（H2O2）诱导大鼠肾上腺嗜铬细胞瘤细胞（PC12）凋亡的影响及机制。方法培养PC12细胞，取对数生长期细胞分为五组，空白对照组、模型组、蜂胶黄酮高、中、低剂量组，剂量分别为200mg/L、100mg/L、50mg/L.药物预处理2h后，孵育H2O2（140μmol/L）24h诱导过氧化损伤。TUNEL试剂盒检测原位细胞凋亡,流式细胞仪检测细胞内活性氧水平以及细胞周期，ELISA检测细胞内Caspase-3蛋白含量。结果TUNEL细胞凋亡染色显示,H2O2组与空白对照
2、组比较染色明显加深,而蜂胶黄酮组染色明显变浅，说明蜂胶黄酮能对抗H2O2诱导细胞凋亡；周期结果显示H2O2组处于G0/G1细胞明显增多，而处于G2/M、S期细胞明显减少，细胞增殖降低，而蜂胶黄酮增加S期细胞促进细胞增殖；与空白对照组相比H2O2组活性氧水平、细胞内Caspase-3含量明显增高，而蜂胶黄酮各剂量组活性氧水平降低，Caspase-3含量减少。结论蜂胶黄酮对H2O2诱发PC12神经细胞凋亡有显著的抑制作用，其机制可能其影响细胞周期、清除氧自由基、降低凋亡因子Caspase-3有关。关键词蜂胶黄酮；PC12细胞；H2O2;Caspase-3；细胞凋亡毕业设计（
3、论文）AbstractObjective: Toobservetheprotectionof propolisflavonoids onratwithinjuriedpheochromocytomacells(PC12)inducedby hydrogenperoxide(H2O2) andtoexploreitspossiblemechanism.Methods: Culture PC12cells,thecellsin thelogarithmicgrowthphasewere dividedintofivegroups,blankcontrolgroup,m
4、odelgroup,propolisflavone ofhigh,mediumandlowdosegroup,thedoseof200mg/L,100mg/L,50mg/L. After2h0f Pharmacologicalpreconditioning,thecells wereincubatedwithH2O2(140μmol/L) for 24h toinduce oxidativedamage. TUNELKit isusedfor determiningCellapoptosis,Flowcytometrywasusedtodetecttheintracel
5、lularROSlevelandcellcycle,ELISAisusedfordeterminingtheconcentrationofproteinCaspase-3incells.Results: ApoptosisofTUNELcellsstaining,H2O2groupcomparedwiththecontrolgroup,stainingwasdeepened,andthepropolisflavonegroupwassignificantlylighter,thatpropolisflavonoidscanantagonizetheapoptosisin
6、ducedbyH2O2CycleshowedthatH2O2groupinG0/G1cellswereincreased,andintheG2/M,Sphasecellsdecreasedsignificantly,reducedcellproliferation,andpropolisflavonoidsincreasedSphasecellspromotingcellproliferation;comparedwiththeblankcontrolgroup,caspase-3inH2O2group,thelevelsofreactiveoxygenspeciesi
7、ncellsincreasedsignificantly,whilethepropolisflavoneinalldosegroupsdecreasethelevelsofreactiveoxygenspecies,reducedcaspase-3content.Conclusion:PropolisflavonoidsonH2O2-inducedPC12cellsdamageasignificantprotectiveeffect,Themechanismmaybeitseffectoncellcycle,scavengingoxyge
