ChemicalConstituentsofMagnoliakobusFruitsandTheirPreventiveEffectsagainstSkeletalMuscleWasting

Abstract

Magnoliakobus는국문명으로목련이라고불리는국내자생식물이다.또한야외에서월동하기때문에국내전역에서널리자라며이는산업적이용에유리할것으로예상된다.국내외에서많은연구가진행되어왔지만대부분은지상부나꽃봉오리에국한되어연구되었다.본연구에서는M.kobus열매로부터화학적성분및골격근소모예방효과를평가하였다. M.kobus열매추출물에서넓은극성범위를갖는화학성분의분리를시도하였고분리동정된화합물들은다음과같다:sesamin(1),kobusin(2),eudesmin(3),cosmosaldehyde(4)scopoletin(5)magnostellinA(6)fagesol(7),piperonylicacid(8)4-hydroxybenzoicacid4-O-glucoside(9),dihydrophaseicacid(10),parabenacid(11),2-hydroxy-5-methoxypyridine(12)magnolosideA(13),magnolosideB(14),rutin(15)sucrose(16),glycerol(17),shikimicacid(18),pinitol(19).또한,2종류의신규pyrazine유도체화합물이분리동정되었고,M.kobus종명을따서kobusininesA(20)andB(21)로명명하였다. 일반적으로골격근위축은다양한질병및노화,유전적요인,신체고정화등여러요인에의한단백질의분해로,삶의질을저하시키는것으로알려져있습니다.이연구에서,공복에의한근관위축증은M.kobus열매의kobusin화합물에대한효과로myosinheavychain을증가시키고단백질분해인자인atrogene(특히MuRF1)의억제를확인하였다.또한Akt의인산화와SIRT1단백질의과발현이kobusin에의해증가되었다.절식동물모델에서atrogene발현의신호전달기전인Akt/FoxO는kobusin에의해유도된FoxO1과FoxO3a인산화를통해MuRF1을억제하여단백질분해를방지하고골격근감소에대한효과를나타낸다. |Magnoliakobus,theplantwidelygrowsalloverKorea,becauseofoverwinteringintheopenair.Thatisfavorablyexpectedwithindustrialuse.Althoughithasbeenstudiedalotathomeandabroad,yetitisusuallylimitedtotheentireaerialpartsorflowerbuds.Inthisstudy,chemicalconstituentsandpreventiveeffectsagainstskeletalmusclewastingwereevaluatedfromthefruitofM.kobus. Intheextract,itwasattemptedthattheseparationofchemicalconstituentswithawidepolarityrange.Thenineteenknowncompoundshavebeenisolatedandreportedasfollows:sesamin(1),kobusin(2),eudesmin(3),cosmosaldehyde(4)scopoletin(5)magnostellinA(6)fagesol(7),piperonylicacid(8)4-hydroxybenzoicacid4-O-glucoside(9),dihydrophaseicacid(10),parabenacid(11),2-hydroxy-5-methoxypyridine(12)magnolosideA(13),magnolosideB(14),rutin(15)sucrose(16),glycerol(17),shikimicacid(18),andpinitol(19).Inaddition,twonovelcompoundsofpyrazinederivativewereisolatedandafterthespeciesnamedkobusininesA(20)andB(21). Ingeneral,itisknownthatskeletalmuscleatrophydeterioratesthequalityoflife,andthatarisesfromthebreakdownofprotein,becauseofseveralfactorsasvariousdiseases,aging,immobilization,andgeneticfactors.Infasting-inducedmyotubeatrophy,therewasconfirmedthattheeffectonkobusinfromM.kobusfruitincreasedmyosinheavychainandinhibitedatrogene(especiallyMuRF1).Inaddition,thephosphorylationofAktandtheincreaseofSIRT1signalingwereincreasedbykobusin.Instarvedmice,Akt/FoxO,asignalingmechanismofatrogeneexpression,inhibitsMuRF1throughkobusin-inducedFoxO1andFoxO3aofphosphorylation,therebypreventingproteindegradationandeffectsagainstskeletalmusclewasting.