纳米雄黄干预肺癌a549细胞对vegf及hif-1表达的影响

《纳米雄黄干预肺癌a549细胞对vegf及hif-1表达的影响》由会员上传分享，免费在线阅读，更多相关内容在学术论文-天天文库。

1、提要目的：探讨纳米雄黄对人肺腺癌A549细胞株血管内皮生长因子（VEGF）、缺氧诱导因子（HIF-1）表达的影响及其抗肿瘤血管生成的机理。方法：采用细胞培养方法，运用免疫组化法、RT-PCR技术观察纳米雄黄对人肺癌A549细胞VEGF、HIF-1的表达的影响，进而探讨纳米雄黄抗肿瘤血管生成的作用机理。结果：实验研究证实，纳米雄黄可以抑制人肺癌A549细胞增殖，随药物浓度的增高作用增强，且与顺铂联合应用有协同作用，初步揭示纳米雄黄抗肿瘤血管生成的机理可能与下调VEGF、HIF-1的表达有关。结论：纳米雄黄可以通过抑制肿瘤细胞血管生成等途径实现抗肿瘤作用，与顺铂联合可产生协同作

2、用。关键词纳米雄黄；肿瘤血管生成；人肺腺癌A549细胞；VEGF；HIF-1ExplorerealgarnanoonhumanlungcancerA549cellsVEGF,HIF-1expressionanditsanti-angiogenicmechanismSpeciality:InternalMedicineofTCMAuthor:YuLianyangTutor:ProfessorQiYuanfuAbstractObjective:ToexplorerealgarnanoonhumanlungadenocarcinomaA549celllineofvasculare

3、ndothelialgrowthfactor(VEGF)andhypoxia-induciblefactor(HIF-1)expressionanditsanti-angiogenicmechanism.Methods:Usingcellculturemethods,theuseofimmunohistochemicalmethods,RT-PCRtechniquetoobserverealgarnanoonhumanlungcancerA549cellsofVEGF,HIF-1expression,andthusexplorethenanometerrealgaranti

4、-angiogenicmechanismofaction.Results:TheexperimentalstudyconfirmedthatrealgarnanocaninhibittheproliferationofhumanlungcancerA549cellswithincreaseddrugconcentration,theenhancedroleofcisplatinsynergy,initiallyrevealednanometerrealgaranti-angiogenicmechanismmaybedownwardadjustmentofVEGF,HIF-1

5、expression.Conclusion：Realgarnanothroughtheinhibitionoftumorcellangiogenesispathwaytoachieveanti-tumoreffectofthesynergisticeffectincombinationwithcisplatin.Keywordsnanometerrealgar;tumorangiogenesis;humanlungadenocarcinomaA549cells;VEGF;HIF-1目录引言...........................................

6、....................................................................................1实验研究...............................................................................................................................21实验材料....................................................................

7、.......................................................22细胞培养...........................................................................................................................33实验分组......................................................................