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1、·248·呻善材JournalofChineseMedicinalMaterial,；第35卷第2期2012年2月·藥理·亞麻木酚素聯(lián)合硼替佐米誘導(dǎo)肺腺癌A549細胞凋亡的機制研究李先偉，楊解人(皖南醫(yī)學(xué)院藥理學(xué)教研室，安徽蕪湖241001)摘要目的：探討亞麻木酚素(SDG)聯(lián)合蛋白酶體抑制劑硼替佐米(Bortezomib，Bor)對肺腺癌A549細胞凋亡的影響及其機制。方法：MTI"法檢測細胞增殖；AnnexinV—FITC／PI雙染流式細胞法和Hoeehst33258熒光染色法檢測細胞凋亡；比色法檢測半胱氨酸天冬氨酸蛋白酶．3(Caspase．3)活性；RealTimePCR檢測Ca
2、spase．3、BCL-2、BAXmRNA的表達；WesternBlot檢測BCL-2、Bax及p-JNK的蛋白表達。結(jié)果：SDG聯(lián)合Bor能明顯抑制細胞生長，上調(diào)Caspase一3活性，促進p-JNK、BAXmRNA和蛋白的表達，抑制BCL-2mRNA和蛋白的表達，誘導(dǎo)細胞凋亡。結(jié)論：SDG聯(lián)合Bor可顯著誘導(dǎo)肺腺癌A549細胞的凋亡，其機制可能與其激活JNK信號通路有關(guān)。關(guān)鍵詞亞麻木酚素；硼替佐米；肺腺癌A549細胞；細胞凋亡中圖分類號：R285．5文獻標(biāo)識碼：A文章編號：100154(2012)02-0248-06EtfiectsofSecoisolariciresinolDigl
3、ucosideCombinedwithB0,rtezomibonInductionofApoptosisinLungCancerCallLineA549LIXian—wei，YANGJie—Fen(Departmentofpharmacology，WannanMedicalCollege，Wuhu241001，China)AbstractObjective：TostudytheinfluenceofSeeoisolariciresinolDiglucoside(SDG)combinedwithBortezomiboninductionofapoptosisinLungCancerCell
4、LineA549anditsrelativemechanisms．Methods：TheeffectonproliferationwasevaluatedbyMTras—say．ThecellapoptosiswasstudiedbyfloweytometryandHoeehst33342staining．ColorimetriemethodwasusedtOdetecttheactivityofCaspase-3．RealTimePCRwasusedtodetecttheexpressionofCaspase-3，BCL-2andBAXmRNA．Westernblotwasusedto
5、de-terminethechangeofp-INK，BCL-2andBAXproteinexpressioninA549cells．Results：Thecellgrowthwassignificantlysloweddownandthecellapoptosiswasinducedafterthecombinedtreatment,．MeanwhiletheCaspase．·3activityandtheexpressionofCaspase一3mRNAwereobviouslyincreased，theexpressionofBCL-2mRNAandproteinweresigni
6、ficantlydownregulatedandtheexpressionofBAX．p-JNKmRNAandproteinweresignificantlyupregulatedafterthecombinedtreatment．Conclusion：TheresultsdemonstratethatSDGcombinedwithBortezomibCansignificantlyinduceapoptosisofA549cells，itsmechanismsmaybeinvolvedinactivationoftheJNKpathway,．KeywordsSeeoisolaricir
7、esinolDiglueoside；Bortezomib；LungCancerCellLineA549；Apoptosis蛋白酶體抑制劑硼替佐米(Bortezomib，Bor)是癌的作用，未見文獻報道，故本研究以A549細胞為新一類的抗腫瘤藥物，能誘導(dǎo)多種腫瘤細胞和癌變研究對象，從細胞和基因水平探討SDG聯(lián)合Bor對細胞凋亡，顯著增強某些化療藥物誘導(dǎo)腫瘤細胞凋非小細胞肺癌的效果和機制。亡的效果，而對于正常細胞的毒性相對較小?。但1材
