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ID:14948024
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页数:5页
时间:2018-07-31
《帕金森病大鼠模型多巴胺转运蛋白125i-β-cit放射自显影研究》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、帕金森病大鼠模型多巴胺转运蛋白125I-β-CIT放射自显影研究 【摘要】目的探讨125I-β-CIT[甲基-3β-(4-碘苯基)托烷-2β-羧酸盐]多巴胺转运蛋白(DAT)显像技术的临床应用价值。方法应用6-羟基多巴胺(6-OHDA)建立黑质部分损毁及完全损毁偏侧帕金森病(PD)大鼠模型。静脉注射125I-β-CIT40μCi进行放射自显影。高效液相-电化学法检测纹状体多巴胺(DA)及其代谢产物含量。免疫组化酪氨酸羟化酶(TH)染色观察黑质及纹状体TH阳性细胞及纤维。结果黑质部分损毁及完全损毁偏侧模型损毁侧纹状体125I-β-
2、CIT放射活性分别为2.67±0.25和0.98±0.29,较未损毁侧分别降低18%和72%,DA含量分别降低39%和98%。TH染色可见损毁侧黑质及纹状体TH阳性细胞及纤维明显少于对侧。结论DAT的显像研究可能有助于PD早期诊断及病情监测。 AutoradiographicstudyofdopaminetransporterinratmodelsofParkinsondiseasewith125I-β-CIT LIUZhenguoCHENShengdi,SUNWenshan,etal DepartmentofNeurolo
3、gy,RuijinHospital,ClinicalandResearchCenterforParkinsonDisease,ShanghaiSecondMedicalUniversity,Shanghai200025.China 【Abstract】ObjectiveTostudythevalueofimagingfordopaminetransporter(DAT)with125I-β-CIT.MethodsTheratmodelsofhemiparkinsonismwitheitherpartialorcompletele
4、sionswererenderedwith6-hydroxydopamine(6-OHDA).Eachratwasinjectedintravenouslywith125I-β-CITcontaining40μCi.Coronaltissuesectionswereimagedbyautoradiography.Thelevelsofdopamine(DA)anditsmetabolitesweremeasuredbyhighperformanceliquidchoromatographyandelectrochemicaldet
5、ection(HPLC-ECD).Thetyrosinehydroxylase(TH)-positivecellsandfibresinthesubstantianigraandstriatumoftheratswereobservedwithimmunohistochemicalstaining.ResultsTheradioactivitiesinthelesionsofthestriatumofbothpartialandcompletehemiparkinsonianlesionsoftheratmodelswere2.6
6、7±0.25and0.98±0.29,respectively,andweresingificantlydecreasedby18%and72%,respectively,ascomparedwiththoseonthesidewithoutlesions.ThelevelsofDAinthelesionsofthestriatumofpartialandcompleteratmodelsweredecreasedby39%and98%,respectively.ThelossofTH-positivecellsandfibres
7、inthesubstantianigraandstriatumwasfoundinthelesionsofthestriatumofbothpartialandcompletehemiparkinsonianratmodels.ConclusionTheimagingstudyofDATmaybehelpfulfortheearlydiagnosisofParkinson′sdiseaseandforthemonitoringoftheprogressionofthisdisease. 【Keywords】Carrierprot
8、eins;Parkinsondisease; 125I-β-CIT;Autoradiography 帕金森病(Parkinsondisease,PD)病理基础是中脑黑质多巴胺(DA)能神经元及黑质纹状体通路变性死亡。中枢多巴胺转运蛋白(DAT)位
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