摘要
Background:Chronicinflammationisanimportantetiologicmechanismformuscleatrophy.Oat-derivedphytochemicalavenanthramides(AVAs)havebeenshowntosuppressinflammatoryresponsesinhumanclinicalstudiesandinseveralcelllinesinvitro,buttheirroleinskeletalmuscleisunclear.TheaimofthisstudywastoinvestigatewhetherAVAtreatmentcanpreventtumornecrosisfactor(TNF)-α-inducedmusclefiberatrophyinC2C12cells.Methods:Wetreated70%confluentcellsfor24hwithAVA.Then,TNF-αwasaddedtocell-culturedmedium.Subsequently,cellswereharvestedatdifferenttimepoints.Thecellswereexaminedusingvariousbiochemicaltechniquesformeasuringprotein,messengerRNAlevels,nuclearbindingactivity,andviability.Fluorescencemicroscopewasusedforanalysisofthemyotubemorphology.Results:CellstreatedwithTNF-asignificantlyincreasednuclearfactorkBactivation,indicatedbyamarkeddecreaseofIkB(p<0.05)anda6.6-foldincreaseinp65-DNAbinding(p<0.01);however,30mmolofAVA-A,-B,and-Ctreatmentreducedthebindingby33%,18%,and19%(p<0.01),respectively,comparedwithcellstreatedwithTNF-awithoutAVA.Theinterleukin-6levelincreasedby2.5fold(p<0.01)withTNF-α,butdecreasedby24%,32%,and28%(p<0.01),respectively,withAVA-A,-B,and-C.Theinterleukin-1blevelalsoshoweda47%increasewithTNF-a(p<0.01),whereasthisincrementwasabolishedinallAVA-treatedcells.Reactiveoxygenspeciesproductionwas1.3-foldhigherintheTNF-α-treatedgroup(p<0.01)butnotintheTNF-α+AVAsgroups.MessengerRNAlevelsofmuscle-specificE3ubiquitinligaseatrogin-1increased23%inTNF-αvs.control(p<0.05)butwasdecreasedby46%,34%,and53%(p<0.01),respectively,withtreatmentofAVA-A,-B,and-C.Moreover,TNF-αtreatmentincreasedthemuscleRINGfinger1messengerRNAlevelby76%(p<0.01);thischangewasabolishedbyAVAs.CellstreatedwithTNF-ademonstratedareducedproliferationcomparedwithcontrolcells(p<0.01)
出版日期
2019年02月12日（中国期刊网平台首次上网日期，不代表论文的发表时间）
