Kupffer cell depletion attenuates superoxide anion release into the hepatic sinusoids after lipopolysaccharicle treatment]

Masahiko Fukuda, Hirokazu Yokoyama, Takeshi Mizukami, Hideki Ohgo, Yukishige Okamura, Yoshitaka Kamegaya, Yoshinori Horie, Shinzo Kato, Hiromasa Ishii

研究成果: Article

22 引用 (Scopus)

抄録

Background and Aim: The mechanisms involved in the beneficial effect of gadolinium chloride against endotoxin-induced liver damage were studied. Methods: Superoxide anions released into the hepatic sinusoids were examined in a liver perfusion model using the cytochrome C method. Results: Gadolinium chloride treatment fully depleted ED2-positive cells from the liver and significantly attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-α (TNF-α) challenge. Moreover, gadolinium chloride treatment resulted in a significant decline in endothelial cell damage in the hepatic sinusoids as assessed by the purine nucleoside phosphorylase/glutamic-pyruvic transaminase ratio in the liver perfusate. Although gadolinium chloride treatment did not affect the level of serum TNF-α, it significantly reduced that of interleukin (IL)-8 and neutrophil migration in the hepatic sinusoids after the lipopolysaccharide challenge. Conclusion: These data suggest that a reduction of the superoxide anion level in the hepatic sinusoids in acute endotoxemia and subsequent reduction of neutrophil migration into the liver may indicate that gadolinium chloride treatment suppresses the progression of liver damage in acute endotoxemia.

元の言語English
ページ(範囲)1155-1162
ページ数8
ジャーナルJournal of Gastroenterology and Hepatology (Australia)
19
発行部数10
DOI
出版物ステータスPublished - 2004

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Kupffer Cells
Superoxides
Liver
Endotoxemia
Lipopolysaccharides
Neutrophils
Tumor Necrosis Factor-alpha
Purine-Nucleoside Phosphorylase
Cytochromes
Alanine Transaminase
Interleukin-8
Endotoxins
Endothelial Cells
Perfusion
gadolinium chloride

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

これを引用

Kupffer cell depletion attenuates superoxide anion release into the hepatic sinusoids after lipopolysaccharicle treatment]. / Fukuda, Masahiko; Yokoyama, Hirokazu; Mizukami, Takeshi; Ohgo, Hideki; Okamura, Yukishige; Kamegaya, Yoshitaka; Horie, Yoshinori; Kato, Shinzo; Ishii, Hiromasa.

:: Journal of Gastroenterology and Hepatology (Australia), 巻 19, 番号 10, 2004, p. 1155-1162.

研究成果: Article

Fukuda, Masahiko ; Yokoyama, Hirokazu ; Mizukami, Takeshi ; Ohgo, Hideki ; Okamura, Yukishige ; Kamegaya, Yoshitaka ; Horie, Yoshinori ; Kato, Shinzo ; Ishii, Hiromasa. / Kupffer cell depletion attenuates superoxide anion release into the hepatic sinusoids after lipopolysaccharicle treatment]. :: Journal of Gastroenterology and Hepatology (Australia). 2004 ; 巻 19, 番号 10. pp. 1155-1162.
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AU - Okamura, Yukishige

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AU - Horie, Yoshinori

AU - Kato, Shinzo

AU - Ishii, Hiromasa

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N2 - Background and Aim: The mechanisms involved in the beneficial effect of gadolinium chloride against endotoxin-induced liver damage were studied. Methods: Superoxide anions released into the hepatic sinusoids were examined in a liver perfusion model using the cytochrome C method. Results: Gadolinium chloride treatment fully depleted ED2-positive cells from the liver and significantly attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-α (TNF-α) challenge. Moreover, gadolinium chloride treatment resulted in a significant decline in endothelial cell damage in the hepatic sinusoids as assessed by the purine nucleoside phosphorylase/glutamic-pyruvic transaminase ratio in the liver perfusate. Although gadolinium chloride treatment did not affect the level of serum TNF-α, it significantly reduced that of interleukin (IL)-8 and neutrophil migration in the hepatic sinusoids after the lipopolysaccharide challenge. Conclusion: These data suggest that a reduction of the superoxide anion level in the hepatic sinusoids in acute endotoxemia and subsequent reduction of neutrophil migration into the liver may indicate that gadolinium chloride treatment suppresses the progression of liver damage in acute endotoxemia.

AB - Background and Aim: The mechanisms involved in the beneficial effect of gadolinium chloride against endotoxin-induced liver damage were studied. Methods: Superoxide anions released into the hepatic sinusoids were examined in a liver perfusion model using the cytochrome C method. Results: Gadolinium chloride treatment fully depleted ED2-positive cells from the liver and significantly attenuated superoxide anion release after a lipopolysaccharide or tumor necrosis factor-α (TNF-α) challenge. Moreover, gadolinium chloride treatment resulted in a significant decline in endothelial cell damage in the hepatic sinusoids as assessed by the purine nucleoside phosphorylase/glutamic-pyruvic transaminase ratio in the liver perfusate. Although gadolinium chloride treatment did not affect the level of serum TNF-α, it significantly reduced that of interleukin (IL)-8 and neutrophil migration in the hepatic sinusoids after the lipopolysaccharide challenge. Conclusion: These data suggest that a reduction of the superoxide anion level in the hepatic sinusoids in acute endotoxemia and subsequent reduction of neutrophil migration into the liver may indicate that gadolinium chloride treatment suppresses the progression of liver damage in acute endotoxemia.

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KW - Neutrophils

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