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  1. C100 医学部/医学系研究科
  2. C100b 紀要
  3. Nagoya journal of medical science
  4. 79(4)

Indole-3-propionic acid suppresses indoxyl sulfate-induced expression of fibrotic and inflammatory genes in proximal tubular cells

https://doi.org/10.18999/nagjms.79.4.477
https://doi.org/10.18999/nagjms.79.4.477
06cf96d1-ad33-4074-bfb7-0082ad9b3e5d
名前 / ファイル ライセンス アクション
07_Yisireyli.pdf 07_Yisireyli.pdf (11.5 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2017-11-22
タイトル
タイトル Indole-3-propionic acid suppresses indoxyl sulfate-induced expression of fibrotic and inflammatory genes in proximal tubular cells
著者 Yisireyili, Maimaiti

× Yisireyili, Maimaiti

WEKO 74127

Yisireyili, Maimaiti

Search repository
Takeshita, Kyosuke

× Takeshita, Kyosuke

WEKO 74128

Takeshita, Kyosuke

Search repository
Saito, Shinichi

× Saito, Shinichi

WEKO 74129

Saito, Shinichi

Search repository
Murohara, Toyoaki

× Murohara, Toyoaki

WEKO 74130

Murohara, Toyoaki

Search repository
Niwa, Toshimitsu

× Niwa, Toshimitsu

WEKO 74131

Niwa, Toshimitsu

Search repository
キーワード
主題Scheme Other
主題 indole-3-propionic acid
キーワード
主題Scheme Other
主題 indoxyl sulfate
キーワード
主題Scheme Other
主題 aryl hydrocarbon receptor
キーワード
主題Scheme Other
主題 TGF-β1
キーワード
主題Scheme Other
主題 proximal tubular cells
抄録
内容記述 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-β1 (TGF-β1) and monocyte chemotactic protein-1 (MCP-1). Furthermore, IS is a potent endogenous agonist for aryl hydrocarbon receptor (AHR), which regulates the transcription of genes such as cytochrome P450 (CYP) 1A1. Indole-3-propionic acid (IPA) is an antioxidant and has been reported to be neuroprotective. We determined whether IPA suppresses IS-induced expression of AHR, CYP1A1, TGF-β1, and MCP-1 in proximal tubular cells. The effects of IS on the expression of AHR, CYP1A1, TGF-β1, and MCP-1 were studied using normotensive rats and hypertensive rats. The effects of IPA on IS-induced expression of AHR, CYP1A1, TGF-β1, and MCP-1 were studied using proximal tubular cells (HK-2). Furthermore, the effects of IPA on IS-induced expression and phosphorylation of signal transducer and activator of transcription 3 (Stat3) were studied in HK-2 cells. Administration of IS induced the expression of AHR, CYP1A1, TGF-β1, and MCP-1 in the tubular cells of rat kidneys. IPA significantly suppressed IS-induced mRNA and protein expression of AHR, CYP1A1, TGF-β1, and MCP-1 in HK-2 cells. IPA suppressed the IS-induced expression and phosphorylation of Stat3 in HK-2 cells. Furthermore, knockdown of Stat3 inhibited the IS-induced mRNA and protein expression of AHR, CYP1A1, TGF-β1, and MCP-1 in HK-2 cells. In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-β1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Thus, IPA suppresses IS-induced expression of fibrotic and inflammatory genes in proximal tubular cells.
内容記述タイプ Abstract
内容記述
内容記述 This study was supported in part by JSPS research grant (JSPS KAKENHI Grant Number 15J00397).
内容記述タイプ Other
出版者
出版者 Nagoya University Graduate School of Medicine, School of Medicine
言語
言語 eng
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
ID登録
ID登録 10.18999/nagjms.79.4.477
ID登録タイプ JaLC
ISSN(print)
収録物識別子タイプ ISSN
収録物識別子 0027-7622
書誌情報 Nagoya Journal of Medical Science

巻 79, 号 4, p. 477-486, 発行日 2017-11
著者版フラグ
値 publisher
URI
識別子 http://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/794.html
識別子タイプ URI
URI
識別子 http://hdl.handle.net/2237/27117
識別子タイプ HDL
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