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《Brivanib对HepG2细胞的抑制作用及机制 优先出版.pdf》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、现代肿瘤医学2017年02月第25卷第03期MODERNONCOLOGY,Feb.2017,VOL.25,NO.03·355·Brivanib对HepG2细胞的抑制作用及机制12韩兴华,王章桂InhibitoryeffectandmechanismofBrivanibonHepG2cells12HanXinghua,WangZhanggui12DepartmentofOncology,TheAffiliatedProvincialHospitalofAnhuiMedicalUniversity,AnhuiHefei230001,China;Departmento
2、fRa-diationOncology,TheSecondPeople'sHospitalofAnhuiProvince,AnhuiHefei230001,China.【Abstract】Objective:ToexploretheinhibitoryeffectandmechanismofBrivanibonhumanhepatocellularcarci-nomaHepG2cells.Methods:Theanti-proliferativeeffectofBrivanibonHepG2cellswereassessedbyMTS.HepG2cellapop
3、tosisratewasdeterminedbyflowcytometry(FCM)analysisaftervariousconcentrationBrivanibtreatment.TheexpressionsofBcl-2andBaxweredetectedbyWesternblot.TheexpressionofLC3wereexaminedbyimmuno-fluorescenceandWesternblot.Results:Theanti-proliferativerateswereincreasedindose-dependantandtime-d
4、ependantmanners.AfterincubatedwithdifferentdosesofBrivanib,theinhibitoryratesofHepG2cellswere(13.06±4.06)%,(20.89±1.83)%and(44.29±2.56)%,respectively.Theapoptosisrateswere(13.06±4.06)%,(20.89±1.83)%and(44.29±2.56)%,respectively.WhichwerecorrelatedwiththedecreasingofBaxandin-creasingo
5、fBcl-2.Furthermore,theexpressionofLC3wasincreasedby2.5μmol/LBrivanibtreatment,andp62de-creased.Conclusion:BrivanibinhibitstheproliferationofHepG2cells,inducesapoptosisandactivatesautophagy.【Keywords】hepatocellularcarcinomacells,Brivanib,apoptosis,autophagyModernOncology2017,25(03):03
6、55-0357【摘要】目的:探讨Brivanib对人HepG2肝癌细胞的增殖抑制作用及其机制。方法:MTS法检测Brivanib对HepG2细胞的增殖抑制作用,流式细胞仪检测不同浓度Brivanib处理后HepG2细胞的凋亡率,Westernblot检测凋亡相关蛋白Bcl-2、Bax的表达情况,免疫荧光观察Brivanib处理后HepG2细胞内源性LC3表达情况,Westernblot检测自噬关键蛋白LC-I向LC-II的转换及p62的表达。结果:与空白对照组相比,Brivanib对HepG2肝癌细胞的增殖抑制率随剂量增加和时间延长而增加,呈剂量和时间依赖性。不
7、同浓度Brivanib作用72h后HepG2细胞的凋亡率分别为(13.06±4.06)%、(20.89±1.83)%、(44.29±2.56)%,其诱导凋亡与下调Bax、上调Bcl-2表达相关。2.5μmol/LBrivanib处理HepG2细胞48h后内源性LC3表达增加。Westernblot分析表明,LC3-I向LC3-II转换增加,p62表达降低。结论:Brivanib抑制HepG2人肝癌细胞增殖,诱导凋亡和自噬活化。【关键词】肝细胞癌;Brivanib;凋亡;自噬【中图分类号】R735.7【文献标识码】ADOI:10.3969/j.issn.1672-
8、4992.2017.03
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