Cattle Bile Aggravates Diclofenac Sodium-Induced Small Intestinal Injury in Mice英文文献资料.docVIP

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Cattle Bile Aggravates Diclofenac Sodium-Induced Small Intestinal Injury in Mice英文文献资料.doc

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Cattle Bile Aggravates Diclofenac Sodium-Induced Small Intestinal Injury in Mice英文文献资料

HindawiPublishingCorporation Evidence-BasedComplementaryandAlternativeMedicine Volume2011,ArticleID315858,8pages doi:10.1155/2011/315858 ResearchArticle CattleBileAggravatesDiclofenacSodium-InducedSmall IntestinalInjuryinMice HironoriIshikawaandShiroWatanabe DivisionofClinicalApplication,InstituteofNaturalMedicine,UniversityofToyama,2630Sugitani,Toyama930-0194,Japan CorrespondenceshouldbeaddressedtoShiroWatanabe,shirowat@inm.u-toyama.ac.jp Received17November2010;Revised17February2011;Accepted18February2011 Copyright?2011H.IshikawaandS.Watanabe. This is an open access article distributed under the Creative Commons AttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkis properlycited. Cattlebile(CB)haslongbeenusedinJapanasaningredientofdigestivemedicines.Bileacidsaremajorchemicalconstituentsof CB,andCBingestionisassumedtoa?ectsmallintestinalinjuryinducedbynonsteroidalanti-in?ammatorydrugs(NSAIDs).Mice werefedadietsupplementedwithorwithoutCBfor7daysandtreatedwithdiclofenacsodium(DIF)toinducesmallintestinal injury.Lesionformationwasenhanced,andPGE2contentandCOXexpressionlevelswereelevatedinthesmallintestineofDIF- treatedmicefedtheCBdietcomparedwiththosefedthecontroldiet.Theadministrationofareconstitutedmixtureofbileacids foundinCBenhancedlesionformationinDIF-treatedmice.CBadministrationelevatedthecontentsofCB-derivedbileacids inthesmallintestine,someofwhichexhibitedahighcytotoxicitytoculturedintestinalepithelialcells.Theseresultssuggestthat theelevatedlevelsofCB-derivedcytotoxicbileacidsinthesmallintestinecontributetotheaggravationofDIF-inducedsmall intestinalinjury.TheuseofCBmaybelimitedduringthetherapyofin?ammatorydiseaseswithNSAIDs. 1.Introduction proin?ammatorycytokines[8].Bacterialtranslocationalso upregulatesCOX-2expression,leadingtothestimulationof prostaglandinsynthesisinthesmallintestine[8].However, thisCOX-2-dependentprostaglandinsynthesisplaysapro- tective role by attenuating the earlier pathologic