AIM:Toinvestigatetheanti-apoptoticcapabilityofthehepatitisBvirus(HBV)intheHepG2hepatomacelllineandtheunderlyingmechanisms.METHODS:CellviabilityandapoptosisweremeasuredbyMTTassayandflowcytometry,respectively.Targetedknockdownofmanganesesuperoxidedismutase(MnSOD),AMP-activatedproteinkinase(AMPK)andhepatitisBvirusXprotein(HBx)genesaswellasAMPKagonistAICARandantagonistcompoundCwereemployedtodeterminethecorrelationsofexpressionofthesegenes.RESULTS:HBVmarkedlyprotectedthehepatomacellsfromgrowthsuppressionandcelldeathintheconditionofserumdeprivation.AdecreaseofsuperoxideanionproductionaccompaniedwithanincreaseofMnSODexpressionandactivitywasfoundinHepG2.215cells.Moreover,AMPKactivationcontributedtotheup-regulationofMnSOD.HBxproteinwasidentifiedtoinducetheexpressionofAMPKandMnSOD.CONCLUSION:OurresultssuggestthatHBVsuppressesmitochondrialsuperoxidelevelandexertsanantiapoptoticeffectbyactivatingAMPK/MnSODsignalingpathway,whichmayprovideanovelpharmacologicalstrategytopreventHCC.
