摘要
Thepurposeofthepresentstudywastodetermineprotectivieeffectsofbasicfibroblastgrowthfactor(bFGF)oncochlearneuronsandhaircellsinvitroandinvivo.InexperimentI,culturedspiralganglionneurons(SGNs)preparedfromP3micewereexposedto20mMglutamatefor2hoursbeforetheculturemediumwasreplacedwithfreshmediumcontaining0,25,50,and100ng/mlbFGF,respectively.Fourteendayslater,allcultureswerefixedwith4%paraformaldehyde,andstainedwith1%toluidineblue.ThenumberofsurvivingSGNswerecountedandthelengthofSGNsneuritesweremeasured.Exposureto20mMglutamatefor24hoursresultedinaninhibitiononneuriteoutgrowthofSGNsandelevatedcelldeath.TreatmentofthecultureswithbFGFledtopromotionofneuriteoutgrowthandelevatednumberofsurvivingSGNs.EffectsofbFGFweredosedependentwiththehighestpotencyat100ng/ml.InexperimentⅡ,invivostudieswerecarriedoutwithguineapigsinwhichbFGForartificialperilymphwasperfusedintothecochleatoassesspossibleprotectiveeffectsofbFGFoncochlearhaircellsandcompoundactionpotentials(CAP).TheCAPsweremeasuredbefore,immediatlyand48hoursafterexposuretonoise.SignificantdifferencesinCAPwereobserved(p＜0.05)amongthebFGFperfusedgroup,controlgroup(t=3.896)andartificialperilymphperfusedgroup(t=2.520)at48hoursafternoiseexposure,CochleaewereremovedandhaircellLosswasanalyzedinsurfacepreparationspreparedfromallexperimentalanimals.Acoustictraumacausedlossof651and687innerhaircellsinthecontrolandartificialperilymphperfusedgroup,respectively.Insharpcontrast,only31innerhaircellswerelostinthebFGFperfusedears.Similarly,moreouterhaircellsdiedinthecontrolandperilymphperfuesedgroup(41830and41968,respectively)thaninthegrouptreatedwithbFGF(34258).OurresultsdemonstratethatbFGFprotectedSGNsagainstglutmateneurotoxicityinvitro.Inaddition,treatmentwithbFGFalso
出版日期
2003年01月11日（中国期刊网平台首次上网日期，不代表论文的发表时间）
