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特異体質性肝障害にアシルCoAチオエステル中間代謝物は関与しているか?
https://kindai.repo.nii.ac.jp/records/21450
https://kindai.repo.nii.ac.jp/records/21450258e79e4-8d75-4802-b490-157f3ddb570c
名前 / ファイル | ライセンス | アクション |
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17K08432seika.pdf (105.5 kB)
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Item type | 研究報告書 / Research Paper(1) | |||||
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公開日 | 2021-03-15 | |||||
タイトル | ||||||
言語 | ja | |||||
タイトル | 特異体質性肝障害にアシルCoAチオエステル中間代謝物は関与しているか? | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Involvement of acyl-CoA thioester metabolite in drug-induced idiosyncratic liver injury | |||||
著者 |
岩城, 正宏
× 岩城, 正宏× 川瀬, 篤史× 島田, 紘明 |
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言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題 | 特異体質性肝毒性, 反応性代謝物, 非ステロイド性抗炎症薬, 免疫細胞 | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
著者(英) | ||||||
en | ||||||
Iwaki, Masahiro | ||||||
著者(英) | ||||||
en | ||||||
Kawase, Atsushi | ||||||
著者(英) | ||||||
en | ||||||
Shimada, Hiroaki | ||||||
著者 所属 | ||||||
近畿大学薬学部; 教授 | ||||||
著者 所属 | ||||||
近畿大学薬学部; 准教授 | ||||||
著者 所属 | ||||||
近畿大学薬学部; 助教 | ||||||
著者所属(翻訳) | ||||||
Kindai University | ||||||
著者所属(翻訳) | ||||||
Kindai University | ||||||
著者所属(翻訳) | ||||||
Kindai University | ||||||
著者 役割 | ||||||
研究代表者 | ||||||
著者 役割 | ||||||
研究分担者 | ||||||
著者 役割 | ||||||
研究分担者 | ||||||
版 | ||||||
出版タイプ | NA | |||||
出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||
出版者 名前 | ||||||
出版者 | 近畿大学 | |||||
書誌情報 |
科学研究費助成事業研究成果報告書 (2019) p. 1-6, 発行日 2020 |
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リンクURL | ||||||
内容記述タイプ | Other | |||||
内容記述 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K08432/ | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 研究成果の概要(和文):非ステロイド性抗炎症薬 (NSAIDs)誘発性の特異体質性肝障害の発症原因の一つとして、肝臓内で生成されるアシルCoAチオエステル体 (NSAID-CoA)に着目し、生合成や化学的合成を試みたが、その生成は確認できなかった。一方で、NSAIDsは微弱ながらもアシルCoA合成酵素 (ACS)に対する阻害活性を有していた。また、肝障害発症原因の一つであるアシルグルクロン酸抱合体 (AG)についても検討し、酵素によるNSAID-AGの分解が特異体質性毒性と関連すること、マクロファージがAG生成を介したNSAIDsの肝細胞毒性発症に寄与することを明らかにした。研究成果の概要(英文):We focused on the acyl-CoA thioester metabolites of NSAIDs (NSAID-CoAs) as one of the cause of NSAID-induced idiosyncratic liver injury. Although we attempted to obtain NSAID-CoAs to evaluate their chemical reactivity, we could not synthesized NSAID-CoAs successfully by performing both biological and chemical experiments. On the other hand, NSAIDs inhibited acyl-CoA synthase activity quite weakly. In addition to NSAID-CoA, we also investigated contribution of acyl glucuronide metabolite of NSAIDs (NASID-AGs) to development of NSAID-induced idiosyncratic liver injury. We clarified that the rate constant of enzymatic degradation of NSAID-AGs in rat liver microsomes well concern with the incidence of idiosyncratic toxicity of parent NSAIDs. Moreover, we demonstrated contribution of macrophage to NSAIDs-induced toxicity through AG generation in hepatocyte. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究種目:基盤研究(C); 研究期間:2017~2019; 課題番号:17K08432; 研究分野:薬物動態学; 科研費の分科・細目: | |||||
資源タイプ(WEKO2) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Research Paper | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf |