| Item type |
学術雑誌論文 / Journal Article_02(1) |
| 公開日 |
2018-08-08 |
| タイトル |
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タイトル |
Prostaglandin I2 suppresses the development of diet-induced nonalcoholic steatohepatitis in mice. |
| 言語 |
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言語 |
eng |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
Kupffer cell |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
NASH |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
oxidative stress |
| 資源タイプ |
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資源タイプ |
journal article |
| 著者 |
粂井, 志麻
結城, 幸一
小島, 文章
柏木, 仁
今道, 力敬
奥村, 利勝
成宮, 周
牛首, 文隆
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| 著者 ローマ字 |
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Kumei, Shima |
| 著者 ローマ字 |
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Yuhki, Koh-ichi |
| 著者 ローマ字 |
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Kojima, Fumiaki |
| 著者 ローマ字 |
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Kashiwagi, Hitoshi |
| 著者 ローマ字 |
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Imamichi, Yoshitaka |
| 著者 ローマ字 |
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Okumura, Toshikatsu |
| 著者 ローマ字 |
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Narumiya, Shuh |
| 著者 ローマ字 |
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Ushikubi, Fumitaka |
| 書誌情報 |
FASEB journal
巻 32,
号 5,
p. 2354-2365,
発行日 2018-05-01
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| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
0892-6638 |
| DOI |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
10.1096/fj.201700590R |
| 識別番号 その他 |
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内容記述タイプ |
Other |
|
内容記述 |
PMID：29247122 |
| 抄録 |
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内容記述タイプ |
Abstract |
|
内容記述 |
Nonalcoholic steatohepatitis (NASH) is a hepatic manifestation of metabolic syndrome. Although the prostaglandin (PG)I2 receptor IP is expressed broadly in the liver, the role of PGI2-IP signaling in the development of NASH remains to be determined. Here, we investigated the role of the PGI2-IP system in the development of steatohepatitis using mice lacking the PGI2 receptor IP [IP-knockout (IP-KO) mice] and beraprost (BPS), a specific IP agonist. IP-KO and wild-type (WT) mice were fed a methionine- and choline-deficient diet (MCDD) for 2, 5, or 10 wk. BPS was administered orally to mice every day during the experimental periods. The effect of BPS on the expression of chemokine and inflammatory cytokines was examined also in cultured Kupffer cells. WT mice fed MCDD developed steatohepatitis at 10 wk. IP-KO mice developed steatohepatitis at 5 wk with augmented histologic derangements accompanied by increased hepatic monocyte chemoattractant protein-1 (MCP-1) and TNF-α concentrations. After 10 wk of MCDD, IP-KO mice had greater hepatic iron deposition with prominent oxidative stress, resulting in hepatocyte damage. In WT mice, BPS improved histologic and biochemical parameters of steatohepatitis, accompanied by reduced hepatic concentration of MCP-1 and TNF-α. Accordingly, BPS suppressed the LPS-stimulated Mcp-1 and Tnf-α mRNA expression in cultured Kupffer cells prepared from WT mice. PGI2-IP signaling plays a crucial role in the development and progression of steatohepatitis by modulating the inflammatory response, leading to augmented oxidative stress. We suggest that the PGI2-IP system is an attractive therapeutic target for treating patients with NASH.-Kumei, S., Yuhki, K.-I., Kojima, F., Kashiwagi, H., Imamichi, Y., Okumura, T., Narumiya, S., Ushikubi, F. Prostaglandin I2 suppresses the development of diet-induced nonalcoholic steatohepatitis in mice. |
| 資源タイプ |
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内容記述タイプ |
Other |
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資源タイプ |
text |
| 著者版フラグ |
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出版タイプ |
AM |
| フォーマット |
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内容記述タイプ |
Other |
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内容記述 |
application/pdf |
| ID(XooNIps) |
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29247122 |
| 閲覧数(XooNIps) |
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| ダウンロード数(XooNIps) |
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286 |
7046.pdf (15.8 MB)
