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Hepatic Sulfotransferase as a Nephropreventing Target by Suppression of the Uremic Toxin Indoxyl Sulfate Accumulation in Ischemic Acute Kidney Injury
http://hdl.handle.net/2298/33281
http://hdl.handle.net/2298/33281adfe2f0d-65ef-40a7-beb8-ff10b9af7545
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ToxSci_Kfu119_FINAL_Ver.pdf (703.7 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2015-10-16 | |||||
| タイトル | ||||||
| タイトル | Hepatic Sulfotransferase as a Nephropreventing Target by Suppression of the Uremic Toxin Indoxyl Sulfate Accumulation in Ischemic Acute Kidney Injury | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題 | Sulfotransferase, indoxyl sulfate, uremic toxin, Nrf2, renal organic anion transporters, resveratrol | |||||
| 資源タイプ | ||||||
| 資源タイプ | journal article | |||||
| 著者 |
Saito, Hideyuki
× Saito, Hideyuki× Yoshimura, Misato× Saigo, Chika× Komori, Megumi× Nomura, Yui× 山本, 裕子× Sagata, Masataka× Wakida, Ayaka× Chuman, Erina× Nishi, Kazuhiko× Jono, Hirofumi |
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| 別言語の著者 |
齋藤, 秀之
× 齋藤, 秀之× 吉村, 美里× 西郷, 智香× 小森, めぐみ× 野村, 祐衣× 山本, 悠子× 佐潟, 雅隆× 脇田, 紋佳× 中馬, 江里奈× 西, 一彦× 城野, 博史 |
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| 内容記述 | ||||||
| 内容記述 | Ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) is evoked by diverse pathophysiological conditions and/or surgical procedures. Here, we evaluated the nephropreventive effect of sulfotransferase (SULT) inhibitors, quercetin and resveratrol, which hamper hepatic indoxyl sulfate (IS) production. I/R of the kidney caused severe renal injury with marked accumulation of serum and renal IS and urinary excretion of kidney injury molecule-1. Oral administration of AST-120 resulted in a significant restoration of kidney injury, suggesting that uremic toxins, which can be suppressed or adsorbed by AST-120 in the intestine, contribute to the progression or development of I/R-induced AKI. Oral administration of resveratrol or quercetin, SULT inhibitors, suppressed IS accumulation, accompanied by significant amelioration of renal dysfunction. The expression of nuclear factor E2-related factor 2 (Nrf2) in the renal nuclear fractions was markedly elevated by renal I/R, but suppressed by treatment with SULT inhibitors. IS is primarily taken up by HK-2 cells derived from human proximal tubular cells via organic anion transporters, which then evokes activation of Nrf2, most likely due to intracellular oxidative stress. Renal basolateral organic anion transporters OAT1 and OAT3, which mediate renal tubular uptake of IS in basolateral membrane, were markedly down-regulated by renal I/R, but restored by SULT inhibitors. Our results suggest that renal accumulation of IS in ischemic AKI induces oxidative stress and downregulation of organic anion transporters resulting in kidney damage, which could be restored to some extent by inhibiting hepatic SULT activity as a nephropreventive target. | |||||
| 書誌情報 |
Toxicological Sciences 巻 141, 号 1, p. 206-217, 発行年 2014-09-17 |
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| ISSN | ||||||
| 収録物識別子 | 10966080 | |||||
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| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11221142 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 関連識別子 | 10.1093/toxsci/kfu119 | |||||
| 権利 | ||||||
| 権利情報 | Oxford University Press | |||||
| フォーマット | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | application/pdf | |||||
| 形態 | ||||||
| 703676 bytes | ||||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 日本十進分類法 | ||||||
| 主題Scheme | NDC | |||||
| 主題 | 499 | |||||
| 出版者 | ||||||
| 出版者 | Oxford University Press | |||||
| 資源タイプ | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 論文(Article) | |||||
| 資源タイプ・ローカル | ||||||
| 雑誌掲載論文 | ||||||
| 資源タイプ・NII | ||||||
| Journal Article | ||||||
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| text | ||||||
| 資源タイプ・ローカル表示コード | ||||||
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| URL | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | http://toxsci.oxfordjournals.org/content/early/2014/06/25/toxsci.kfu119.abstract | |||||
| コメント | ||||||
| This is a pre-copy-editing, author-produced PDF of an article accepted for publication in Toxicological Sciences following peer review. The definitive publisher-authenticated version Toxicological Sciences 2014 141：206-217 is available online at: http://toxsci.oxfordjournals.org/content/early/2014/06/25/toxsci.kfu119.abstract | ||||||
