DDP凋亡机制探索.pdf

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1、四川大学学医学版JSidi2012；43(3)：335-339chuanUniv，MedSciEdi)。。●。‘。姜黄素促卵巢癌耐药细胞株CoC1／DDP凋亡机制探索*林琳，王平△，赵晓兰四川大学华西第二医院妇产科(成都610041)【摘要】目的研究姜黄素对耐药卵巢癌细胞的促凋亡作用及其可能的机理。方法用MTT法检测不同浓度姜黄素、化疗药物[顺铂(DDP)，紫杉醇]及姜黄素联合化疗药物(姜黄素+顺铂，姜黄素+紫杉醇)作用于卵巢癌耐药细胞株c0C1／DDP细胞48h后各组的细胞抑制率，并用流式细胞仪

2、检测上述各组细胞的凋亡率。RT—PCR技术检测姜黄素、顺铂、姜黄素+顺铂作用于COC1／DDP细胞48h后各组的磷脂酰肌醇3一激酶催化亚基(PI3KCA)mRNA的表达。结果不同浓度姜黄素作用COC1／DDP48h后，细胞的抑制率和凋亡率随着姜黄素浓度的升高相应增高，姜黄素联合化疗药物作用组比单用化疗药物组的细胞抑制率及细胞凋亡率高(P<0．05)。顺铂与姜黄素联合用药与顺铂单独作用相比PI3KCAmRNA的表达降低(P

3、用可能与姜黄素和化疗药物协同诱导该细胞系的凋亡有关，其机制可能为降低PI3KCA基因的表达。【关键词】卵巢癌c0c1／DDP姜黄素顺铂细胞凋亡磷脂酰肌醇3一激酶催化亚基StudyonCurcumin-inducedApoptosisinOvarianCancerResistantCellLinesCOC1／DDPLINLin，WANGPing，ZHAOXiao—lan．DepartmentofObstetricsandGynecology，WestChinaSecondHospital，Sichu

4、anUniversity，Chengdu610041，China△C0rresp0ndingauthor，E—mai1：wangping886@126．corn一[Abstract]ObjectiveToinvestigatetheeffectandpossiblemechanismofcurcumintoinduceapoptosisinovariancancerresistanteelllinesC0C1／DDP．MethodsCOC1／DDPcellsweretreatedwithdiffe

5、rentconcentrationofcurcumin，withorwithoutthecombinationofchemotherapydrugscisplatin(DDP)andpaclitaxel(PIX)for48hours．ThegrowthinhibitionratesofCOC1／DDPcellswerestudiedbyMTTmethod，andtheapoptoticratiosweremeasuredwithflowcytometry．Theexpressionofphosph

6、oinositide3-kinasecatalyticsubunit(PI3KCA)mRNAwasstudiedbyRT-PCRincurcumintreatedceils，DDPtreatedcellsandtheircombinationtreatedcells．ResultsAfterthetreatmentofdifferentconcentrationofcurcuminfor48hours，thegrowthinhibitionratesandtheapoptoticrateofCOC

7、l／DDPcellsweregraduallyincreasedaccordinglywithincreasingcurcuminconcentration．Furthurmore，curcuminincombinationwithchemotherapydrugobtainedhigherinhibitionrateandapoptosisratethansinglechemotherapydrugdid(P

8、llstreatedwithcurcumincombinedDDPwasmuchlowerthanthattreatedonlywithDDP(P％O．05)．ConclusionCurcumincanincreasetheapoptoticrateofCOC1／DDPcells，SOhassynergisticeffectonwithchemotherapydrugsontheinductionofcellapoptosis．Itspossiblemechanismmaybere