摘要
AIM:Toinvestigatetheeffectandmechanismofstimulationofthehypothalamicparaventricularnucleuswithglutamateacidinratswithulcerativecolitis(UC).METHODS:Theratswereanesthetizedwith10%chloralhydrateviaabdominalinjectionandtreatedwithanequalvolumeofTNBS+50%ethanolenema,injectedintotheuppersectionoftheanuswiththetailfacingup.Colonicdamagescoreswerecalculatedafterinjectingacertaindoseofglutamicacidintotheparaventricularnucleus(pVN),andtheeffectofthenucleustractussolitarius(NTS)andvagusnerveinalleviatingUCinjurythroughchemicalstimulationofthepVNwasobservedinrats.ExpressionchangesofC-myc,Apaf-1,caspase-3,interleukin(IL)-6,andIL-17duringtheprotectionagainstUCinjurythroughchemicalstimulationofthepVNinratsweredetectedbyWesternblot.Malondialdehyde(MDA)contentandsuperoxidedismutase(SOD)activityincolontissuesofratsweremeasuredbycolorimetricmethods.RESULTS:ChemicalstimulationofthePVNsignificantlyreducedUCinratsinadose-dependentmanner.TheprotectiveeffectsofthechemicalstimulationofthepVNonratswithUCwereeliminatedafterchemicaldamagetothepVN.AfterglutamatereceptorantagonistkynurenicacidwasinjectedintothepVN,theprotectiveeffectsofthechemicalstimulationofthepVNwereeliminatedinratswithUC.AfterAVpVlreceptorantagonist([Deamino-penl,val4,D-Arg8]-vasopressin)wasinjectedintoNTSorbilateralchemicaldamagetoNTS,theprotectiveeffectofthechemicalstimulationofpVNonUCwasalsoeliminated.AfterchemicalstimulationofthepVN,SODactivityincreased,MDAcontentdecreased,C-mycproteinexpressionsignificantlyincreased,caspase-3andApaf-1proteinexpressionsignificantlydecreased,andIL-6andIL-17expressiondecreasedincolontissuesinratswithUC.CONCLUSION:ChemicalstimulationofthehypothalamicpVNprovidesaprotectiveeffectagainstUCinjuryinrats.HypothalamicpVN,NTSandvagusnerveplayk
出版日期
2016年12月22日(中国Betway体育网页登陆平台首次上网日期,不代表论文的发表时间)