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《木犀草素對對乙酰氨基酚誘導(dǎo)的l02肝細(xì)胞損傷的保護(hù)作用》由會員上傳分享，免費在線閱讀，更多相關(guān)內(nèi)容在學(xué)術(shù)論文-天天文庫。
1、木犀草素對對乙酰氨基酚誘導(dǎo)的L02肝細(xì)胞損傷的保護(hù)作用［摘要］探討木犀草素（luteolin，Lirt）對對乙酰氨基酚（acetaminophen,APAP）誘導(dǎo)的L02肝細(xì)胞損傷的保護(hù)作用。CCK8法檢測Lilt對L02細(xì)胞活性的影響；篩選APAP誘導(dǎo)L02細(xì)胞損傷的濃度及作用時間；細(xì)胞形態(tài)學(xué)、CCK8實驗和流式細(xì)胞術(shù)檢測分析Lut對APAP誘導(dǎo)的L02細(xì)胞凋亡的影響；比色法檢測細(xì)胞上清液中丙二醛（MDA）含量、谷胱甘肽（GSH）及超氧化物歧化酶（SOD）活性；RTPCR檢測凋亡相關(guān)基因Bax,Bcl2,caspase3的表達(dá)。結(jié)果顯示Lut在2.5?40umol?L-l不影響L02
2、細(xì)胞活性；12mmol?L-lAPAP作用于L02細(xì)胞12h可用于建立肝細(xì)胞損傷模型。與模型組相比，Lut組細(xì)胞狀態(tài)明顯改善，胞體增大，貼壁能力恢復(fù)明顯；細(xì)胞凋亡率明顯下降；MDA含量顯著下降（P〈0.05或P〈0.01）,GSH和SOD活性顯著提高（P〈0.05或P〈0.01）,同吋能夠上調(diào)Bcl2及下調(diào)Bax,caspase3mRNA的表達(dá)（P〈0.05或P〈0.01）。該實驗證明了Lut對APAP誘導(dǎo)的L02細(xì)胞損傷有保護(hù)作用，其機(jī)制可能與其減輕氧化應(yīng)激反應(yīng)和抑制細(xì)胞凋亡有關(guān)。［關(guān)鍵詞］木犀草素；對乙酰氨基酚；L02細(xì)胞；氧化應(yīng)激；細(xì)胞凋亡Protectiveeffectsofl
3、utcolinagainstacctaminophcninduccddamageinL02livercellsHELanzhi1,3,MENGYakun2,3,HANYanzhong3,ZHANGZhcnfang3,YINPing2,3,SANGXiuxiu3,XIAOXiaohe3*，BAIZhaofang3*(1.SchoolofPharmacy,HunanUniversityofTraditionalChineseMedicine,Changsha410208,China；2.SchoolofPharmacy,JiangxiUniversityofTraditionalChine
4、seMedicine,Nanchang330004,China；3.ChinaMilitaryInstituteofChineseMedicine,302MilitaryHospital,Beijing100039,China)[Abstract]Thispaperwasaimedtoinvestigatetheprotectiveeffectsofluteolin(Lut)againstacetaminophen(APAP)induceddamageinL02livercells.CCK8wasusedtodetectthecellactivationofL02cellstreate
5、dbydifferentLut.TheconcentrationandtimeofAPAPinducedL02celldamagewasscreened.TheeffectofLutonAPAPinducedapoptosisofL02cellswasdetectedbycellmorphologicalobservation,CCK8assayandflowcytometry.ThecontentsofMDA,GSHandSODactivityincellsupernatantweredetectedbycolorimetricassay.Theexpressionofapoptos
6、isrelatedgenesBax,Bcl2andcaspase3wasdetectedbyRTPCR.TheresultsshowedthatLutin2.540pm()l?L-lrangedoesnotaffecttheactivityofL02cells；12mmol?L-lAPAPincubatedwithL02cell12htoestablishdamagemodel.Comparedwiththemodelgroup,thecellstatusofLutgroupwassignificantlyimproved,thecellbodywasincreased,theadhe
7、renceabilitywasrecovered,andtheapoptosisratewasobviouslydecreased.MDAcontentdecreasedsignificantly(P［Keywords］luteolin；acetaminophen；L02cells;oxydatvestress；apoptosisdoi：10.4268/cjcmm20162224對乙酰氨基酚(acetaminophen,APAP)是一種常見的解
