| セッション情報 | International Forum 1(Gastrointestinal tract) 3.Pathogenesis of NSAIDs-enteropathy |
|---|---|
| タイトル | IF1-3-III (Plenary presentation) Involvement of reactive oxygen species in indomethacin-induced apoptosis of small intestinal epithelial cells |
| 演者 | Tatsushi Omatsu（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1） |
| 共同演者 | Yuji Naito（Dept of Medical ProteomicsKyoto Prefectural University of MedicineKyotoJapan^2）, Osamu Handa（Dept of Biomedical Safety ScienceKyoto Prefectural University of MedicineKyotoJapan^3）, Ikuhiro Hirata（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Satoko Adachi（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Tetsuya Okayama（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Etsuko Kishimoto（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Satomi Akagiri（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Takahiro Suzuki（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Tomohisa Takagi（Dept of Biomedical Safety ScienceKyoto Prefectural University of MedicineKyotoJapan^3）, Satoshi Kokura（Dept of Biomedical Safety ScienceKyoto Prefectural University of MedicineKyotoJapan^3）, Hiroshi Ichikawa（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1）, Norimasa Yoshida（Dept.of Molecular Gastroenterology and HepatologyKyoto Prefectural University of MedicineKyotoJapan^4）, Toshikazu Yoshikawa（Dept.of Inflammation and ImmunologyKyoto Prefectural University of MedicineKyotoJapan^1） |
| 抄録 | Background ： Recent progress of endoscope in small intestine made us aware the adverse effects of non-steroidal anti-inflammatory drugs （NSAIDs）such as indomethacin （IND）on small intestinal mucosa． Butthe precise pathogenic mechanism of this phenomenon is still unknown．Aim ： ln the present studywe investigated the mechanism by which IND induced mucosal injury by us-ing an in vitro model of small intestine．Materials and Methods ： Colon cancer cell lineCaco-2exhibiting a small intestinal phenotype starting asa crypt cell and differentiating to a vMous phenotype was employed． IND was added to differentiatedCaco-2 monolayer and the cell death of Caco-2 was quantified by MTT assay and LDH release in the cellculture supernatant． IND-’induced cell death was also qualified by fluorescent probes under fluorescentmicroscope． As a functional studythe permeability of Caco-2 monolayer was assessed by measuring tran-sepithelial electrical resistance （TER） and the flux of FITC-Dextran across the monolayers． IND-inducedreactive oxygen species production in Caco-2 was evaluated by redox-sensitive fluorogenic probes usingfluorometer． ln some experimentsanti-oxidants were used to clarify the role of ROS on IND-induced celldeath．Results ： IND caused cell death （mainly apoptosis） of Caco-2 in dose- and time- dependent manners thatwere correlated with increased permeability of Caco-2 monolayer． Exposure of Caco-2 with IND also re-sulted in a significant ROS production that was inhibited by the pretreatment of these cells with anti-oxi-dants．Conclusion ： Taken togetherROS production is one of the mechanisms by which IND induced small in-testinal injury． |
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