简介：Inthisstudy,weaimedtoexploretheroleofursolicacidintheneuralregenerationoftheinjuredsciaticnerve.BALB/cmicewereusedtoestablishmodelsofsciaticnerveinjurythroughunilateralsciaticnervecompletetransectionandmicroscopicanastomosisat0.5cmbelowtheischialtuberosity.Thesuccessfullygeneratedmodelmiceweretreatedwith10,5,or2.5mg/kgursolicacidviaintraperitonealinjection.Enzyme-linkedimmunosorbentassayresultsshowedthatserumS100proteinexpressionlevelgraduallyincreasedat1-4weeksaftersciaticnerveinjury,andsignificantlydecreasedat8weeks.Assuch,ursolicacidhasthecapacitytosignificantlyincreaseS100proteinexpressionlevels.Real-timequantitativePCRshowedthatS100mRNAexpressionintheL4-6segmentsontheinjurysidewasincreasedafterursolicacidtreatment.Inaddition,themuscularmassindexinthesoleusmusclewasalsoincreasedinmicetreatedwithursolicacid.Toluidinebluestainingrevealedthatthequantityandaveragediameterofmyelinatednervefibersintheinjuredsciaticnerveweresignificantlyincreasedaftertreatmentwithursolicacid.10and5mg/kgofursolicacidproducedstrongereffectsthan2.5mg/kgofursolicacid.Ourfindingsindicatethatursolicacidcandose-dependentlyincreaseS100expressionandpromoteneuralregenerationinBALB/cmicefollowingsciaticnerveinjury.
简介：Thisstudyaimedtoexploretheroleofmechanicaltensioninhypertrophicscarsandthechangeinnervedensityusinghematoxylin-eosinstainingandS100immunohistochemistry,andtoobservetheexpressionofnervegrowthfactorbywesternblotanalysis.Theresultsdemonstratedthatmechanicaltensioncontributedtotheformationofahyperplasticscarinthebackskinofrats,inconjunctionwithincreasesinbothnervedensityandnervegrowthfactorexpressioninthescartissue.Theseexperimentalfindingsindicatethatthecutaneousnervoussystemplaysaroleinhypertrophicscarformationcausedbymechanicaltension.
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