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1、中國(guó)公共衛(wèi)生2014年6月第3O卷第6期ChinJPublicHealth，Jun2014Vo1．30No．6·753··實(shí)驗(yàn)研究·黃芪甲苷對(duì)脂多糖誘導(dǎo)肝細(xì)胞損傷保護(hù)作用佟宇，王晶摘要：目的觀察黃芪甲苷(AslV)對(duì)脂多糖誘導(dǎo)體外培養(yǎng)肝細(xì)胞損傷的保護(hù)作用及其可能機(jī)制。方法將原代培養(yǎng)大鼠肝細(xì)胞分為對(duì)照組，模型組和低、中、高黃芪甲苷(16、32、64／xmol／L)組，作用24h后，噻唑藍(lán)法檢測(cè)細(xì)胞存活率，上清液測(cè)谷草轉(zhuǎn)氨酶(AST)、谷丙轉(zhuǎn)氨酶(ALT)活性，酶聯(lián)免疫吸附法測(cè)定腫瘤壞死因子(TNF一僅)，白細(xì)胞介素_6(IL-6)水平
2、，Westernblot測(cè)定肝細(xì)胞中p65、IKBtx表達(dá)。結(jié)果與對(duì)照組比較，模型組細(xì)胞存活率下降34．9％，AST、ALT活性增高，TNF-僅，IL-6含量增加，p65表達(dá)增高65．9％，IKBoL表達(dá)降低34．5％；與模型組比較，32、64~mol／L黃芪甲苷組細(xì)胞存活率(分別為38．9％和48．1％)升高，AST、ALT活性降低，TNF．，IL．6水平降低，p65表達(dá)降低35．6％和57．8％，而IKBo~表達(dá)增高56．1％和89．2％。結(jié)論黃芪甲苷對(duì)脂多糖誘導(dǎo)的肝細(xì)胞損傷具有保護(hù)作用，且這種保護(hù)作用可能與黃芪甲苷抑制核因子一
3、KB通路進(jìn)而降低炎癥因子表達(dá)有關(guān)。關(guān)鍵詞：肝細(xì)胞損傷；脂多糖；黃芪甲苷；核因子一KB中圖分類(lèi)號(hào)：R512．7文獻(xiàn)標(biāo)志碼：A文章編號(hào)：1001—0580(2014)06—0753—03DOI：l0．11847／zgggws2014—30—06一l8EfectsofastragalosideIVonlip0p0lysaccharide—inducedhepatocytesin-juryinvttroTONGYu，WANGJing(FistAfiliatedHospitalofLiaoningMedicalUniversity，Jinzh
4、ou，LiaoningProvince121000，China)Abstract：0bjeetiveTostudytheprotectiveeffectofastragalosideIV(AsIV)onlipopolysaccharide(LPS)一in—ducedhepatocytesinjuryandtoexploreitspossiblemechanism．MethodsTheculturedhepatocytesweredividedinto5groups：normalgroup，modelgroup，anddifferen
5、tdoesofAslVgroups(16，32，and64i~moL／L)．After24hoursofincu—bation，thecellviabilityratesweredetectedby(3一(4，5-dimethylthiazol一2y1)一2，5diphenyleterazoliumbromide(MTT)as—say．Theactivityofserumaspartateaminotransferase(AST)andalanineaminotransferase(ALT)weredetected．Thecon—t
6、entoftumornecrosisfactor(TNF—)andinterleukin一6(IL-6)weredeterminedbyenzyme—linkedimmunosorbentassay(ELISA)．Theexpressionofp65andIKBoLweremeasuredbyWesternblot．ResultsComparedwiththenormalgroup，thecellviabilityratewasdecreasedby34．9％，thecontentsofALT，AST，TNF—，andIL一6wer
7、eincreasedandtheex—pressionofp65wasincreasedby65．9％．whiletheexpressionofIKBawasdecreasedby34．5％．AslVatdosesof32and64p,mol／LcouldobviouslyreducetheactivitiesofAI，AST，thecontentofTNF-0【，IL-6andtheexpressionofp65(35．6％and57．8％)，increasethetheexpressionofIKBet(56．1％and89．2
8、％)andceltviabilityrates(38．9％and48．1％、comparedwiththoseofthemodelgroup．ConclusionAsIVhasaprotectiveeffectonLPS—induce
