简介：AIM:Toinvestigatetheeffectsofhydrogen-richsaline(HRS)onmicrogliaactivationandSirtuintype1(Sirt1)inratswithN-methyl-N-nitrosourea(MNU)-inducedretinitispigmentosa(RP).METHODS:Ratsweredividedintonorm(N)group,model(M)groupandHRS(H)group.RatsinMandHgroupsweregivensalineandHRSrespectivelypriortoandafteradministrationofMNU.Atoneday(d1)andd3afterwards,electroretinogramandhistologicalexaminationwereperformedtoconfirmtheeffectsofHRSonretinalfunctionandstructureofMNU-inducedRP.Immunofluorescencestainingofanti-ionizedcalcium-bindingadaptermolecule1(Iba1),amakerofmicrogliacells,wasperformed,withquantitativereal-timepolymerasechainreaction(qRT-PCR)foritsmRNAquantification.Moreover,Sirt1mRNAandproteinexpressionintheretinasweredetectedbyWesternblotandqRT-PCR.RESULTS:HRSpreservedtheretinalfunctionandmitigatedthereductionofphotoreceptordegenerationinMNU-treatedretinas.ThepresenceofmicrogliacellswassomewhatmoreobviousinHgroupthanthatinMgroupatd1.HRSsuppressedthefurtheractivationofmicrogliacells,withthenumberofmicrogliacellslessthanthatofMgroupatd3.ResultsofqRT-PCRofIba1wereconsistentwiththoseofimmunofluorescencestaining,withthemRNAexpressionofIba1inHgroupmoreintensivethanthatofMgroupatd1(P<0.05),whilelessthanthatofMgroupatd3(P<0.05).Furthermore,theSirt1mRNAandproteinexpressiondecreasedafterMNUadministration,whileHRSmitigatedtheMNU-induceddownregulationofSirt1.CONCLUSION:HRScaneffectivelykeepmicrogliaactivationinducedbyMNUtoanappropriateextent,whileupregulateSirt1inMNU-inducedRP.