Fractionation of a Herbal Antidiarrheal Medicine Reveals Eugenol as an Inhibitor of Ca2+-Activated Cl？ Channel TMEM16A 英文参考文献.docVIP

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Fractionation of a Herbal Antidiarrheal Medicine Reveals Eugenol as an Inhibitor of Ca2+-Activated Cl？ Channel TMEM16A 英文参考文献.doc

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FractionationofaHerbalAntidiarrhealMedicineRevealsEugenolasanInhibitorofCa2-ActivatedCl？ChannelTMEM16A英文参考文献

FractionationofaHerbalAntidiarrhealMedicineReveals 2 2+ EugenolasanInhibitorofCa -ActivatedCl Channel TMEM16A ZhenYao1,WanNamkung1,2,EunA.Ko1,JinhongPark2,LukmaneeTradtrantip1,A.S.Verkman1* 1Departments of Medicine and Physiology, University of California San Francisco, San Francisco, California, United States of America, 2Yonsei University, College of Pharmacy,YonseiInstituteofPharmaceuticalSciences,Incheon,Korea Abstract The Ca2+-activated Cl2 channel TMEM16A is involved in epithelial fluid secretion, smooth muscle contraction and neurosensory signaling. We identified a Thai herbal antidiarrheal formulation that inhibited TMEM16A Cl2 conductance. C18-reversed-phaseHPLCfractionationoftheherbalformulationrevealed.98%ofTMEM16Ainhibitionactivityinoneout ofapproximately20distinctpeaks.Thepurified,activecompoundwasidentifiedaseugenol(4-allyl-2-methoxyphenol),the majorcomponentofcloveoil.EugenolfullyinhibitedTMEM16ACl2 conductancewithsingle-siteIC50,150mM.Eugenol inhibition of TMEM16A in interstitial cells of Cajal produced strong inhibition of intestinal contraction in mouse ileal segments.TMEM16ACl2channelinhibitionaddstothelistofeugenolmoleculartargetsandmayaccountforsomeofits biologicalactivities. Citation:YaoZ,NamkungW,KoEA,ParkJ,TradtrantipL,etal.(2012)FractionationofaHerbalAntidiarrhealMedicineRevealsEugenolasanInhibitorofCa2+- ActivatedCl2 ChannelTMEM16A.PLoSONE7(5):e38030.doi:10.1371/journal.pone.0038030 Editor:StevenBarnes,DalhousieUniversity,Canada ReceivedJanuary31,2012;AcceptedApril30,2012;PublishedMay30,2012 Copyright:?2012Yaoetal.Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsunrestricted use,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding: This work was supported by National Institutes of Health grants DK72517, HL73856, DK35124, DK86125, EB00415, and EY13574 and Research DevelopmentProgramandDrugDiscoverygrantsfromtheCysticFibrosisFoundation.Th