Beraprost sodium, a prostacyclin (PGI2) analogue, ameliorates concanavalin A-induced liver injury in mice

Satoshi Ohta, Makoto Nakamuta, Marie Fukushima, Motoyuki Kohjima, Kazuhiro Kotoh, Munechika Enjoji, Hajime Nawata

研究成果: ジャーナルへの寄稿記事

14 引用 (Scopus)

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
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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beraprost
Epoprostenol
Concanavalin A
Liver
Wounds and Injuries
Interferons
Tumor Necrosis Factor-alpha
Alanine Transaminase
Interleukin-6
Laser-Doppler Flowmetry
Acute Liver Failure
Blood Circulation
Liver Failure
Blood Volume
Pulmonary Hypertension

All Science Journal Classification (ASJC) codes

  • Hepatology

これを引用

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

Ohta, Satoshi ; Nakamuta, Makoto ; Fukushima, Marie ; Kohjima, Motoyuki ; Kotoh, Kazuhiro ; Enjoji, Munechika ; Nawata, Hajime. / Beraprost sodium, a prostacyclin (PGI2) analogue, ameliorates concanavalin A-induced liver injury in mice. :: Liver International. 2005 ; 巻 25, 番号 5. pp. 1061-1068.
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abstract = "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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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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