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1、中國骨質(zhì)疏松雜志2014年7月第20卷第7期ChinJOsteoporos,July2014,Vol20,No.7750PublishedonlineWWW.wanfangdate.con1.cndoi:10.3969/j.issn.1006-7108.2014.07.007·論著·甲狀旁腺激素聯(lián)合辛伐他汀對成骨細胞分化及OPG和RANKLmRNA表達的影響盧蕾陽劉冰高飛楊靜山西醫(yī)科大學(xué)第一醫(yī)院內(nèi)分泌科,山西太原030001中圖分類號:R681文獻標識碼:A文章編號:1006.7108(2014)
2、07—074505摘要:目的聯(lián)合甲狀旁腺激素(rhPTH)和辛伐他汀(SIM)在體外對乳鼠顱蓋骨成骨細胞分化及骨保護素(OPG)和核因子KB受體活化因子配體(RANKL)基因表達的影響。方法以乳鼠成骨細胞為體外試驗?zāi)P停瑀hPTH1—34(10mol/L)聯(lián)合不同濃度SIM(1O~、1O~、10mol/L)作用于體外培養(yǎng)的乳鼠成骨細胞,采用對硝基苯磷酸鹽(PNPP)法測定堿性磷酸酶(ALP)活性;RT—PCR法測定OPG和RANKL基因的表達。結(jié)果rhPTH和SIM單獨給藥均可促進成骨細胞ALP活
3、性及OPG基因、降低RANKL基因表達(P<0.05);兩者聯(lián)合后與SIM單獨作用組比較,ALP活性明顯增加,并能協(xié)同促進OPG、降低RANKL基因表達(P<0.05)。結(jié)論rhPTH1-34和SIM聯(lián)合應(yīng)用對成骨細胞分化和代謝有協(xié)同作用。關(guān)鍵詞:甲狀旁腺激素;辛伐他汀;成骨細胞;堿性磷酸酶;骨保護素;核因子.cB受體活化因子配體EffectofparathyroidcombinedwithsimvastatinonthedifferentiatiOnofosteoblastsandthemRNA
4、expressionofOPGandRANKLLULeiyang,LIUBing,GAOFei,YANGJingDepartmentofEndocrinology,theFirstHospitalofShanxiMedicalUniversity,Taiyuan030001,ChinaCorrespondingauthor:GAOFei,Email:gaofxixi@126.comAbstract:ObjectiveToobservetheeffectofparathyroid(rhPTH1—34
5、)combinedwithsimvastatin(SIM)onthedifferentiationofosteoblastsandthemRNAexpressionofOPGandRANKLinvitro.MethodsTheneonatalratosteoblastswereculturedinvitro.Theosteoblastsweretreatedwith10一mol/LrhPTH1—34combinedwithdifferentconcentrationsofSIM(10~mol/L,
6、10。mol/L,and10~mol/L,respectively).TheactivityofALPwasassessedusingPNPPcolorimetricassay.ThemRNAexpressionofOPGandRANKLwasdetectedusingsemi—quantitiveRT—PCR.ResultsSingleuseofrhPTH1-34orSIMpromotedALPactivity,increasedtheexpressionofOPG,andreducedthee
7、xpressionofRANKL(P<0.05).ComparedwiththatinsingleSIMtreatmentgroup,theALPactivityinrhPTH1—34combinedwithSIMtreatmentgroupincreasedmoresignificantly,andtheexpressionofOPGwasalsopromoted,whiletheexpressionofRANKLwasdown—regulated(P<0.05).ConclusionrhPTH
8、1—34combinedwithSIMhasadditiveeffectonthedifferentiationandmetabolismofosteoblasts.Keywords:PTH;SIM;Osteoblast;ALP;OPG;RANKL骨質(zhì)疏松癥(Osteoporosis,OP)目前已成為全球汀(Simvastatin,SIM)屬于3一羥基一3甲基戊二酰輔酶性的公共衛(wèi)生問題之一,研究表明改造后的重組人A(HMG—COA)還原酶抑制劑,能減少膽固醇合成及甲狀旁腺激素1—3