| セッション情報 |
International Forum 1(Gastrointestinal tract) 2.Pathogenesis of NSAIDs-gastropathy
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| タイトル |
IF1-2-I (Keynote lecture) Harmful and anti-inflammatory action of NSAID in the stomach
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| 演者 |
Kazuhide Higuchi（2nd Department of Internal MedicineOsaka Medical CollegeTakatsukiJapan） |
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| 抄録 |
NSAIDs and Helicohacter pylori infection are major causes of gastric mucosal damage． Main effect ofNSAIDs is suppression of cyclooxygenase （COX）which produce prostaglandins from arachidonic acid．Prostaglandins play important roles in gastric mucosal defense and repair in the stomachand are also in－duced by the inflammatory change such as chronic gastritis associated with H． pylori． Animal and humanstudies indicate that suppression of COX activity by NSAIDs induces acute gastric mucosal inj ury． lnhibi－tion of COX－2 delays healing of gastric ulcers． Howeverthe effect of long－term NSAIDs administrationon chronic gastritis associated with H． pylori in human beings remains unclear．Our study demonstrated that long－term use of NSAIDs attenuates neutrophil infiltration into gastric mu－cosaoverexpression of iNOSand acceleration of cell turnover of gastric epithelium induced by Hpyloriinfection． H． pylori－induced gastritis is histologically characterized by infiltration of inflammatory cells in－cluding neutrophils into gastric mucosa．1レ8 has been suggested as one of the key proinflammatory cy－tokines attracting neutrophils into gastric mucosa during H． pylori－induced gastritis． We found thatNSAIDs inhibit neutrophil infiltration into gastric mucosa during Hpylori infection． ln vitro study showsinhibitory effect of NSAIDs on 1レ8 induction by H． pylori in gastric epithelial cells． These results suggestthat inhibition of IL－8 by NSAIDs is one of the mechanisms by which long－term NSAIDs attenuates neu－trophil infiltration into gastric mucosa during H． pylori infection．Cell turnover is defined as ratio of cell proliferation and apoptosis and acceleration of cell turnover is oneof the causes of carcinogenesis． Long－term NSAIDs administration inhibits apoptosis and proliferation． ltis reported that COX－2 is overexpressed in gastric cancer and NSAIDs reduce the risk of gastric canceras well as colorectal cancer． One possible mechanism by which NSAIDs inhibit gastric carcinogenesis isthat NSAIDs inhibit gastritis－derived COX． Other possibility is that NSAIDs inhibit gastric carcinogenesisvia inhibition of gastric mucosal inflammation． |
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