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1、人參皂苷Rg1抑制白血病細(xì)胞K562增殖并誘導(dǎo)分化的分子機(jī)制柯大智1，王紅寧2，陳地龍2，顧恒偉2，王亞平2，王建偉2，龍軒3，李春莉4（400016重慶，重慶醫(yī)科大學(xué):附屬第二醫(yī)院老年病科1,組織學(xué)與胚胎學(xué)教研室2，護(hù)理學(xué)院3，生命科學(xué)研究院4)[摘要]目的研究人參皂苷的重要單體Rg1對(duì)人白血病細(xì)胞K562的增殖抑制作用并誘導(dǎo)其向成熟分化的分子機(jī)制。方法取對(duì)數(shù)生長(zhǎng)期K562細(xì)胞，分設(shè)人參皂苷Rg1組和常規(guī)培養(yǎng)組，以流式細(xì)胞儀檢測(cè)各時(shí)間點(diǎn)24、48、72hRg1對(duì)K562細(xì)胞增殖的影響；Wright’s染色測(cè)定細(xì)胞形態(tài)和酶
2、標(biāo)儀測(cè)定血紅蛋白合成來(lái)觀察Rg1作用24、48、72h后各時(shí)間點(diǎn)K562細(xì)胞向成熟細(xì)胞分化的特征；激光共聚焦顯微鏡檢測(cè)Rg1作用48h對(duì)K562細(xì)胞STAT5蛋白分布的影響；Westernblot法檢測(cè)Rg1作用24、48、72h后各時(shí)間點(diǎn)K562細(xì)胞STAT5蛋白表達(dá)的影響。結(jié)果請(qǐng)列出統(tǒng)計(jì)學(xué)分析結(jié)果，P
3、62細(xì)胞體積縮小,核直徑減小,核和漿的比例降低,細(xì)胞向成熟方向分化；激光共聚焦顯微鏡顯示經(jīng)Rg1誘導(dǎo)后,K562細(xì)胞胞漿中的STAT5熒光強(qiáng)度增加，而胞核內(nèi)STAT5熒光強(qiáng)度減弱；Westernblot法檢測(cè)顯示Rg1作用K562細(xì)胞后，細(xì)胞漿內(nèi)STAT5的表達(dá)水平增加，細(xì)胞核內(nèi)STAT5的表達(dá)水平減少，作用48h變化最明顯。結(jié)論人參皂苷單體Rg1可抑制人慢性粒細(xì)胞白血病K562細(xì)胞增殖并誘導(dǎo)其向成熟方向分化；Rg1改變K562細(xì)胞中STAT5的分布和減少K562胞核中STAT5的表達(dá)，這可能是Rg1抑制K562細(xì)胞增殖并
4、誘導(dǎo)其分化的作用機(jī)制之一。[關(guān)鍵詞]人參總皂苷單體Rg1；K562細(xì)胞；增殖抑制；誘導(dǎo)分化；stat[中圖法分類(lèi)號(hào)][文獻(xiàn)標(biāo)志碼]AStudyonthemolecularmechanismsofginsenosideRg1oninhibitoryProliferationanddifferentiationofchronicmyelocyticleukemiaK562cellsKeDazhi1,WangHongning2，ChenDilong2etal請(qǐng)列出所有作者(400016Chongqing,ChongqingMed
5、icalUniversity:DepartmentofGeriatricsCardiology，theSecondAffiliatedHospitalofChongqing,DepartmentofHistologyandEmbryology)[Abstract]ObjectiveToinvestigatetheeffectandmolecularmechanismsofginsenosideRg1oninhibitoryProliferationanddifferentiationofchronicmyelocyticl
6、eukemiaK562cells．MethodsInhibitoryproliferationofK562cellsbyginsenosideRg1wasmeasuredbyflowcytometry(FCM)after24h、48h、72h;ThecharacteristicsofK562celldifferentiationintoerythroidcellswasmeasuredbyWright’sstainingandhemoglobinometry;Theexpressionanddistrictionofsig
7、naltransduoerandactivatoroftranscription5(STAT5)ink562cellsinducedbyRg1weredetectedbyWesternblottingandlaserConfocalassay.ResultsTheSphaseofK562cellinducedbyRg1increased,andreachpeakat48hinFCM;HemoglobininK562cellsinducedbygensingnosideRg1increasedsignificantlyP<0
8、.05；,andGensingnosideRg1couldinducetheK562celIdifferentiationintoerythroidcells,andthemorphologicalfeatureofK562cellspresenteddiminishedvolume，reducednu
