| JaLCDOI | 10.18926/AMO/48564 |
|---|---|
| フルテキストURL | 66_3_245.pdf |
| 著者 | Okada, Toshiaki| Takigawa, Nagio| Kishino, Daizo| Katayama, Hideki| Kuyama, Shouichi| Sato, Ken| Mimoto, Junko| Ueoka, Hiroshi| Tanimoto, Mitsune| Kiura, Katsuyuki| |
| 抄録 | Cisplatin is used to treat lung cancer;however, it is also a known carcinogen. Cyclooxygenase-2 (COX-2) inhibitors have been shown to prevent carcinogen-induced experimental tumors. We investigated the effect of a COX-2 inhibitor, celecoxib, on cisplatin-induced lung tumors. One hundred twenty 4-week-old A/J mice were divided into 6 groups:group 1, no treatment;group 2, low-dose celecoxib (150mg/kg);group 3, high-dose celecoxib (1,500mg/kg);group 4, cisplatin alone;group 5, cisplatin plus low-dose celecoxib;and group 6, cisplatin plus high-dose celecoxib. Mice in groups 4-6 were administered cisplatin (1.62mg/kg, i.p.) once a week for 10 weeks between 7 and 16 weeks of age. All mice were sacrificed at week 30. Tumor incidence was 15.8% in group 1, 25% in group 2, 26.3% in group 3, 60% in group 4, 50% in group 5, and 50% in group 6. Tumor multiplicity was 0.2, 0.3, 0.3, 1.3, 1.0, and 0.6 in groups 1-6, respectively. Tumor multiplicity in the cisplatin-treated mice was reduced by celecoxib treatment in a dose-dependent manner (p＜0.05, group 4 vs. group 6). Celecoxib significantly reduced COX-2 expression in cisplatin-induced tumors (p＜0.01, group 4 vs. group 6). |
| キーワード | cisplatin non-small cell lung cancer celecoxib cyclooxygenase-2 chemoprevention |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2012-06 |
| 巻 | 66巻 |
| 号 | 3号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 245 |
| 終了ページ | 251 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2012 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 22729105 |
| Web of Science KeyUT | 000305669700008 |
| JaLCDOI | 10.18926/AMO/48687 |
|---|---|
| フルテキストURL | 66_4_329.pdf |
| 著者 | Matsushita, Koki| Mizushima, Takaaki| Shirahige, Akinori| Tanioka, Hiroaki| Sawa, Kiminari| Ochi, Koji| Tanimoto, Mitsune| Koide, Norio| |
| 抄録 | The relationship between pancreatic fibrosis and apoptosis of pancreatic acinar cells has not been fully elucidated. We reported that taurine had an anti-fibrotic effect in a dibutyltin dichloride (DBTC)-chronic pancreatitis model. However, the effect of taurine on apoptosis of pancreatic acinar cells is still unclear. Therefore, we examined apoptosis in DBTC-chronic pancreatitis and in the AR42J pancreatic acinar cell line with/without taurine. Pancreatic fibrosis was induced by a single administration of DBTC. Rats were fed a taurine-containing diet or a normal diet and were sacrificed at day 5. The AR42J pancreatic acinar cell line was incubated with/without DBTC with taurine chloramines. Apoptosis was determined by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. The expression of Bad and Bcl-2 proteins in the AR42J cells lysates was detected by Western blot analysis. The apoptotic index of pancreatic acinar cells in DBTC-administered rats was significantly increased. Taurine treatment inhibited pancreatic fibrosis and apoptosis of acinar cells induced by DBTC. The number of TUNEL-positive cells in the AR42J pancreatic acinar cell lines was significantly increased by the addition of DBTC. Incubation with taurine chloramines ameliorated these changes. In conclusion, taurine inhibits apoptosis of pancreatic acinar cells and pancreatitis in experimental chronic pancreatitis. |
| キーワード | apoptosis chronic pancreatitis pancreatic acinar cells taurine |
| Amo Type | Original Article |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2012-08 |
| 巻 | 66巻 |
| 号 | 4号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 329 |
| 終了ページ | 334 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2012 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 22918205 |
| Web of Science KeyUT | 000307918900005 |
| 関連URL | http://ousar.lib.okayama-u.ac.jp/metadata/49739 |
| JaLCDOI | 10.18926/AMO/49251 |
|---|---|
| フルテキストURL | 67_1_1.pdf |
| 著者 | Nishimori, Hisakazu| Maeda, Yoshinobu| Tanimoto, Mitsune| |
| 抄録 | Graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic stem cell transplantation. Chronic GVHD often presents with clinical manifestations that resemble those observed in autoimmune diseases. Standard treatment is 1-2mg/kg/day of prednisone or an equivalent dose of methylprednisolone, with continued administration of a calcineurin inhibitor for steroid sparing. However, the prognosis of steroid-refractory chronic GVHD remains poor. Classically, chronic GVHD was said to involve predominantly Th2 responses. We are now faced with a more complex picture, involving possible roles for thymic dysfunction, transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF), B cells and autoantibodies, and Th1/Th2/Th17 cytokines, as well as regulatory T cells (Tregs), in chronic GVHD. More detailed research on the pathophysiology of chronic GVHD may facilitate the establishment of novel strategies for its prevention and treatment. |
| キーワード | chronic GVHD Th17 Am80 regulatory T cell (Treg) steroid-refractory |
| Amo Type | Review |
| 出版物タイトル | Acta Medica Okayama |
| 発行日 | 2013-02 |
| 巻 | 67巻 |
| 号 | 1号 |
| 出版者 | Okayama University Medical School |
| 開始ページ | 1 |
| 終了ページ | 8 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| 資料タイプ | 学術雑誌論文 |
| 言語 | 英語 |
| 著作権者 | CopyrightⒸ 2013 by Okayama University Medical School |
| 論文のバージョン | publisher |
| 査読 | 有り |
| PubMed ID | 23439503 |
| Web of Science KeyUT | 000316829900001 |