2、以未加壓組作為對照,用四唑鹽法(MTT法)和流式細胞技術分別檢測各組標本在加壓3h和加壓24h后細胞增殖、凋亡的情況*應用硫酸#咔唑法檢測各組標本在加壓3h和加壓24h后蛋白多糖的含量。(結果)加壓3h后,各加壓組與對照組相比,細胞的增殖+凋亡以及蛋白多糖含量無明顯變化*加壓24h后,壓力值為20kPa時可以明顯擬制增殖,并誘導髁突軟骨細胞發(fā)生凋亡增加,蛋白多糖含量明顯減少。(結論)長時間的異常壓力負荷可使髁突軟骨細胞增殖減緩、凋亡增加,蛋白多糖含量減少,誘發(fā)或加重關節(jié)軟骨退變。關鍵詞:關節(jié)軟骨;髁狀突;壓力;細胞外基質(zhì)中圖分類號:R246.83文獻標識碼:
3、A文章編號:1672#3554($%&5)&’#&()(#%’!"#$%&"’()*+,-,.’/)012&33.)")"42)$.*(2-,.)"5’,.6.,7851)1,)3.38-"9:-,2.;<2),&)=$7’-"3+7",>&3.3."?)"97$-2?-2,.$-=&?>)"92)’7,&3!"#$%&’LIAOMing#ting,ZHANGZhi#guang,SUKai,KUANGShi#jun,ZHANGJuan(DepartmentofSurgery,SchoolofGuanghuaStomatology,S*+Yat#,enUniv
4、ersity,Guangzhou510055,China)5@3,2-’,A(Objective)Toinvestigatetheeffectofstaticcompressionontheproliferationactivity,apoptosisrate,andmatrixproteoglycanssynthesisinculturedmandibularcondylarcartilage(MCC)cells,andtherelationbetweenabnormalcompressionanddegradationofcartilage.(Metho
5、ds)MCCcellsofsecondgenerationwereplacedintosealedcontainers,whichwereperfusedwith5%CO2tooffer10kPa,20kPa,#10kPastaticcompressionsrespectively.Nomechanicalloadingwereappliedtothecontrolgroup.Whenthemechanicalloadinglasted3hoursand24hours,theproliferationactivityandtheapoptosisratewe
6、redeterminedbyMTTmethodandflowcytometryrespectively,thecontentofmatrixproteoglycansweredeterminedbysulfuricacid#carbazolecolorimetrymethods.(Results)Whenthepeakstresscameto20kPaandlastmorethan24hours,itcansignificantlydecreaseproliferationactivityandthesynthesisofmatrixproteoglycan
7、s,increasetheapoptosisratesignificantly.(Conclusion)Abnormalcompressioncouldinducetheapoptosisofchondrocytesandreductioninthecontentofproteoglycans,whichmaytriggerordeterioratethedegradationofcartilage.B(7C)293D-rticularjoint;mandibularcondylar;compression;extracellularmatrix[JSUNY
8、at#senUniv(MedSci),2005,26
