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  1. 0 資料タイプ別
  2. 03 紀要論文
  1. 250 大学院医歯学総合研究科(医)
  2. 20 紀要
  3. 02 新潟医学会雑誌
  4. 第109巻第7号

Clostridium difficile toxin 起因性下痢症における細胞内情報伝達機構と消化吸収障害の検討 : Cholera toxin 起因性下痢症と対比して

http://hdl.handle.net/10191/42516
http://hdl.handle.net/10191/42516
d9e4e450-81ab-41e3-aa96-0cda009e166c
名前 / ファイル ライセンス アクション
109(7)_340-352.pdf 109(7)_340-352.pdf (1.9 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2016-07-08
タイトル
タイトル Clostridium difficile toxin 起因性下痢症における細胞内情報伝達機構と消化吸収障害の検討 : Cholera toxin 起因性下痢症と対比して
タイトル
言語 en
タイトル Clostridium difficile toxin 起因性下痢症における細胞内情報伝達機構と消化吸収障害の検討 : Cholera toxin 起因性下痢症と対比して
言語
言語 jpn
キーワード
主題Scheme Other
主題 clostridium difficile toxin
キーワード
主題Scheme Other
主題 digestion and absorption disturbance
キーワード
主題Scheme Other
主題 intracellular signal transduction
キーワード
主題Scheme Other
主題 brush border membrane enzyme
キーワード
主題Scheme Other
主題 inositolphosnholipid turnover
キーワード
主題Scheme Other
主題 クロストリディウム ディフィシルトキシン
キーワード
主題Scheme Other
主題 消化吸収障害
キーワード
主題Scheme Other
主題 細胞内情報伝達機構
キーワード
主題Scheme Other
主題 刷子縁膜酵素
キーワード
主題Scheme Other
主題 イノシトールリン脂質代謝回転
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
その他のタイトル
その他のタイトル Study of Intracellular Signal Transduction and of Digestion and Absorption Disturbance in Clostridium Difficile Toxin-Induced Diarrhea : Comparison with Those in Cholera Toxin-Induced Dirrhea
著者 中澤, 俊郎

× 中澤, 俊郎

WEKO 115701

中澤, 俊郎

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著者別名
識別子 115702
識別子Scheme WEKO
姓名 Nakazawa, Toshiro
抄録
内容記述タイプ Abstract
内容記述 The mechanism of diarrhea induced by Clostridium difficile (CD) toxin is not fully understood although that by Cholera toxin is sufficiently done. Present experiment aims to clarify its mechanism. Male Wistar rats weighing about 200 g were used, and CD toxin were injected into the lumen of ligated jejunal loops. First, time course study of histological examination and measurement of fluid accumulation in the ligated loops were carried out from 2 to 10 hours after CD toxin exposure. Second, we studied the changes of the activities of microvillus membrane enzymes and intestinal absorption rates of oligopeptides. Third, we studied the changes of activities of two intracellular mediators, protein kinase C (PKC) which is activated by diacylglycerol, and inositol 1-4-5-trisphosphate (IP_3) which releases Ca^<++> from endoplasmic reticulum. Diacyiglycerol and IP_3 are produced by receptor mediated-inositolphospholipid turnover. Luminal fluid accumulation steadily increased from 2 to 10 hours after CD toxin exposure. Slight damage in villus tips was observed 2 hours after exposure, and the change became more severe with time. Leucine aminopeptidase (LAP) activity was significantly decreased at 2 hours. The absorption rates of peptides were markedly decreased in toxin treated rats as compared with control rats using the jejunal perfusion method. Activity of PKC was significantly increased at 30 minutes, and that of IP_3 was also increased 1 hour after CD toxin exposure. In addition, PKC antagonist, staurosporin, inhibited the toxin induced-fluid accumulation. Calmodulin antagonists, trifluoperazine and chlorpromazine, also inhibited it. These results indicate that CD toxin increased inositolphospholipid turnover with subsequent activation of PKC and IP_3 in epithelial cell. Then inositolphospholipid turnover and Ca^<++> mobilization possibly play a synergistic role in inhibition of LAP and peptide carrier protein synthesis. Consequently inhibition of LAP synthesis and disturbance of peptide absorption may partly contribute to the CD toxin induced diarrhea.
書誌情報 新潟医学会雑誌
en : 新潟医学会雑誌

巻 109, 号 7, p. 340-352, 発行日 1995-07
出版者
出版者 新潟医学会
ISSN
収録物識別子タイプ ISSN
収録物識別子 00290440
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00182415
著者版フラグ
値 publisher
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