抄録
Background/Aims: Prostacyclin (PGI2) is a potent mediator in the inflammatory and coagulation processes. The aim of this study was to test whether beraprost sodium, a PGI2 analogue, could prevent experimental hepatic injury induced by concanavalin A (Con A), which is a model of fulminant hepatic failure. Methods: Beraprost (100 μg/kg) was administered intraperitoneally simultaneously with Con A (40 mg/kg) in C57B6J mice. Blood circulation in the liver was determined by laser-Doppler flowmetry. Plasma levels of alanine aminotransferase (ALT), tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6 were determined. Levels of TNF-α and IFN-γ in culture supernatant of splenocytes were also determined. Results: Beraprost administration reduced the incidence of death following hepatic failure (76.5% vs. 29.4%, P<0.05). Plasma levels of ALT were significantly lower in the beraprost-treated group than in the control group, and in the former, there was concomitant suppression of the histological features of injury. Beraprost significantly increased hepatic blood flow volume in Con A-treated mice. Plasma levels of TNF-α and IFN-γ were significantly reduced at 6 and 12h after Con A injection, respectively, but the levels of IL-6 were increased at 6h. In vitro, beraprost also suppressed Con A-induced TNF-α production in splenocytes, while it stimulated IFN-γ production. Conclusion: These findings imply that beraprost suppresses Con A-induced liver injury. These data also suggest that beraparost, which is clinically effective in treating pulmonary hypertension, may have therapeutic potential for preventing hepatic injury.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 1061-1068 |
| ページ数 | 8 |
| ジャーナル | Liver International |
| 巻 | 25 |
| 発行部数 | 5 |
| DOI | |
| 出版物ステータス | 出版済み - 10 1 2005 |
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All Science Journal Classification (ASJC) codes
- Hepatology
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Beraprost sodium, a prostacyclin (PGI2) analogue, ameliorates concanavalin A-induced liver injury in mice. / Ohta, Satoshi; Nakamuta, Makoto; Fukushima, Marie; Kohjima, Motoyuki; Kotoh, Kazuhiro; Enjoji, Munechika; Nawata, Hajime.
：: Liver International, 巻 25, 番号 5, 01.10.2005, p. 1061-1068.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Beraprost sodium, a prostacyclin (PGI2) analogue, ameliorates concanavalin A-induced liver injury in mice
AU - Ohta, Satoshi
AU - Nakamuta, Makoto
AU - Fukushima, Marie
AU - Kohjima, Motoyuki
AU - Kotoh, Kazuhiro
AU - Enjoji, Munechika
AU - Nawata, Hajime
PY - 2005/10/1
Y1 - 2005/10/1
N2 - Background/Aims: Prostacyclin (PGI2) is a potent mediator in the inflammatory and coagulation processes. The aim of this study was to test whether beraprost sodium, a PGI2 analogue, could prevent experimental hepatic injury induced by concanavalin A (Con A), which is a model of fulminant hepatic failure. Methods: Beraprost (100 μg/kg) was administered intraperitoneally simultaneously with Con A (40 mg/kg) in C57B6J mice. Blood circulation in the liver was determined by laser-Doppler flowmetry. Plasma levels of alanine aminotransferase (ALT), tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6 were determined. Levels of TNF-α and IFN-γ in culture supernatant of splenocytes were also determined. Results: Beraprost administration reduced the incidence of death following hepatic failure (76.5% vs. 29.4%, P<0.05). Plasma levels of ALT were significantly lower in the beraprost-treated group than in the control group, and in the former, there was concomitant suppression of the histological features of injury. Beraprost significantly increased hepatic blood flow volume in Con A-treated mice. Plasma levels of TNF-α and IFN-γ were significantly reduced at 6 and 12h after Con A injection, respectively, but the levels of IL-6 were increased at 6h. In vitro, beraprost also suppressed Con A-induced TNF-α production in splenocytes, while it stimulated IFN-γ production. Conclusion: These findings imply that beraprost suppresses Con A-induced liver injury. These data also suggest that beraparost, which is clinically effective in treating pulmonary hypertension, may have therapeutic potential for preventing hepatic injury.
AB - Background/Aims: Prostacyclin (PGI2) is a potent mediator in the inflammatory and coagulation processes. The aim of this study was to test whether beraprost sodium, a PGI2 analogue, could prevent experimental hepatic injury induced by concanavalin A (Con A), which is a model of fulminant hepatic failure. Methods: Beraprost (100 μg/kg) was administered intraperitoneally simultaneously with Con A (40 mg/kg) in C57B6J mice. Blood circulation in the liver was determined by laser-Doppler flowmetry. Plasma levels of alanine aminotransferase (ALT), tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6 were determined. Levels of TNF-α and IFN-γ in culture supernatant of splenocytes were also determined. Results: Beraprost administration reduced the incidence of death following hepatic failure (76.5% vs. 29.4%, P<0.05). Plasma levels of ALT were significantly lower in the beraprost-treated group than in the control group, and in the former, there was concomitant suppression of the histological features of injury. Beraprost significantly increased hepatic blood flow volume in Con A-treated mice. Plasma levels of TNF-α and IFN-γ were significantly reduced at 6 and 12h after Con A injection, respectively, but the levels of IL-6 were increased at 6h. In vitro, beraprost also suppressed Con A-induced TNF-α production in splenocytes, while it stimulated IFN-γ production. Conclusion: These findings imply that beraprost suppresses Con A-induced liver injury. These data also suggest that beraparost, which is clinically effective in treating pulmonary hypertension, may have therapeutic potential for preventing hepatic injury.
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U2 - 10.1111/j.1478-3231.2005.01143.x
DO - 10.1111/j.1478-3231.2005.01143.x
M3 - Article
VL - 25
SP - 1061
EP - 1068
JO - Liver International
JF - Liver International
SN - 1478-3223
IS - 5
ER -