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1、D-木糖苷对HepG2细胞的细胞毒性及其作用机制24-O-乙酰升麻醇-3-D-D-木糖苷对HepG2细胞的细胞毒性及其作用机制田泽,斯建勇,王婷,杨梦避.,韩锐,肖培根(1.中国医学科学院.中国协和医科大学药用植物研究所,北京100094;2.香港城市大学深圳研究院,广东深圳518057;3.中国医学科学院一中国协和医科大学药物研究所,北京100050)摘要:目的研究24.0.乙酰升麻醇.3.o-,8一D.木糖苷对HepG2细胞的细胞毒性及其作用机制.方法利用MTF法进行细胞毒活性初筛;用荧光染色细胞
2、形态学观察法,流式细胞术和蛋白质杂交技术从细胞和分子水平研究该化合物的细胞毒作用机制.结果24.O.乙酰升麻醇-3.O-/3.D.木糖苷可以抑制HepG2细胞生长,Ic5o值为13t~mol?L～.该化合物可以诱导HepG2细胞凋亡和G,/M细胞周期阻滞.进一步分子水平研究表明,该化合物可使PARP蛋白裂解,抗凋亡蛋白bcl2下调,凋亡蛋白Bax上调,细胞周期素cyclinB和细胞周期素依赖性激酶cdc2表达下调.结论24.O.乙酰升麻醇-3.o-/3一D.木糖苷通过诱导细胞凋亡和G,/M细胞周期阻滞
3、来发挥细胞毒作用,其凋亡机制涉及caspases家族激活,bcl2下调和Bax表达上调,而G2/M周期阻滞与cdc2和cyclinB下调直接相关.关键词:24.O.乙酰升麻醇-3.D.D.木糖苷;凋亡;细胞形态;细胞周期;蛋白表达中图分类号:R965文献标识码:A文章编号:1001—2494(2007)07—0505—05CytotoxicityandMechanismof24?O?Acetylcimigenolo3?O-D?XylopyranosideonHepG2CellsTIANZe,SIJia
4、n.yong,WANGTing,YANGMeng.su,HANRui,XIAOPei.gen'(1.InstitHteofMedicinalPlant,ChineseAcademyofMedicalSciences,PekingUnionMedicalCollege,Beijing100094,China;2.DepartmentBiologyandChemistry,CityUniversityo厂ttongKong,Shenzhen518057,China;3.InstituteMateriaMe
5、dica,ChineseAcademyMedicalSciences,PekingUnionMedicalCollege,Beijing100050,China)ABSTRACT:OBJECTIVEToelucidatethecytotoxicityandmechanismof24?O.acetyIcimigenoI.3?O-/3一D?xylopyranosideonHepG2cells.METHODSMTF,AO/EBfluorescencestainingobservation,flowcytom
6、etryandwesternblotmethodswereusedtostudythecy?totoxicity,morphologicalchanges,cellcycledistributionandproteinexpressionprofileof24?O?acetylcimigenol一3?o-/3?D-xylopyranosideonHepG2cells.RESULTS24.0.acetylcimigenolo3.o-/3-D.xylopyranosideinhibitedtheproli
7、ferationofHepG2cellswithIC∞at13LLmo1.L～,andinducedapoptosisandG2/Mcellcyclearrest.FurtherstudydemonstratedthatthecompoundcleavagedPARP,down-regulatedtheantiapoptoticproteinexpressionofbcl2,up?regulatedtheapoptoticproteinexpressionofBax,decreasedtheexpre
8、ssionofcyclinandcyclindependentkinasecyclinBandcdc2.CONCLUSION24.0一acetylcimigenol?3?o-/3-D-xylopyranosideexertsitscyto—toxicitvonHepG2cellsviaapoptosisandG,/Marrest.Inaddition,caspasesfamilyactivation,thedown?regulationofbcl2and
