BETA-glucuronidase and chloroacetate-esterase staining discriminates rat liver sinusoidal endothelial cells from Kupffer cells in primary culture

Schlayer, H.‐J.; Woort-Menker, M.; Eyhorn, S.; Becker, Heiko; Schaefer, Hans E.; Decker, Karl

doi:10.1007/bf02896579

Virchows Archiv B Cell Pathol

1988

DOI: 10.1007/bf02896579

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BETA-glucuronidase and chloroacetate-esterase staining discriminates rat liver sinusoidal endothelial cells from Kupffer cells in primary culture

H.‐J. Schlayer

M. Woort-Menker

S. Eyhorn

et al.

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Cited by 2 publications

References 12 publications

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The Fibrin-Derived Peptide Bβ15-42 Attenuates Liver Damage in a Rat Model of Liver Ischemia/Reperfusion Injury

Liu¹,

Fang

Yang³

et al. 2013

Shock

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The inflammatory response after liver ischemia/reperfusion (I/R) contributes to increased risk of liver failure after liver surgery. Strategies aimed to preventing inflammation could be beneficial in reducing liver I/R injury. Recent studies have demonstrated that peptide Bβ15-42 is able to decrease the injury of I/R in heart and kidney by inhibition of leukocyte migration and preserving endothelial barrier function. Prompted by these results, we hypothesized that Bβ15-42 could also possess anti-inflammatory abilities to protect from or reduce hepatic I/R injury. Therefore, in this study, we aimed to evaluate the effects of Bβ15-42 in a model of liver I/R injury in rats. Rats were treated with Bβ15-42 at initiation of reperfusion and 2 h thereafter. Rats were killed at 0.5, 6, 24, and 48 h after reperfusion. Hepatic mRNA levels of fibrinogen-α (Fgα), Fgβ, Fgγ were significantly increased after I/R. Treatment with Fg-derived Bβ15-42 ameliorated liver I/R injury, as indicated by lower serum aminotransferase levels and fewer I/R-associated histopathologic changes. Bβ15-42 treatment decreased leukocyte infiltration and expression of hepatic inflammatory cytokines. Moreover, Bβ15-42 significantly reduced high-mobility group box 1 release and altered mitogen-activated protein kinase activation. In conclusion, Bβ15-42 treatment protected against liver warm I/R injury. The mechanism of protective action of Bβ15-42 seemed to involve its ability to reduce hepatic inflammatory response through preventing high-mobility group box 1 release and altering mitogen-activated protein kinase activation.

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The Fibrin-Derived Peptide Bβ15-42 Attenuates Liver Damage in a Rat Model of Liver Ischemia/Reperfusion Injury

Liu¹,

Fang

Yang³

et al. 2013

Shock

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Cytokines, nitric oxide synthesis and liver regeneration

Decker

Obolenskaya

1995

J of Gastro and Hepatol

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During the prereplicative period of liver regeneration the changes in the levels of mRNA for tumour necrosis factor-alpha (TNF-alpha) and its receptors were nearly synchronous. The mRNA levels reached their maximum 1-3 h after operation and exceeded the values for intact animals about ten-fold. Lipopolysaccharide stimulation induced an increase in TNF-alpha and TNF receptor production comparable with that occurring during regeneration. Nitric oxide (NO) production in the regenerating liver was determined by electron paramagnetic resonance (EPR) spectroscopy. The first increase in NO production occurred approximately 1 h after partial hepatectomy (PHE). The second and more pronounced peak of NO production was observed about 6 h after PHE when the hepatocytes entered the first cell cycle; it originated mainly from these cells. The consequent minimum of NO synthesis coincided with the maximal rate of DNA synthesis. The third gradual rise of NO production was seen at the transit from the first to the second cell cycle of the hepatocytes and the entrance of the non-parenchymal cells into proliferation. Hepatocytes, Kupffer and endothelial cells were isolated from livers after PHE. They were found to start their main NO production in the described sequence at the times corresponding to their respective entrance into the cell cycle. The maxima of NO synthesis were inversely correlated to the DNA-synthesizing activity of the individual cell type.

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BETA-glucuronidase and chloroacetate-esterase staining discriminates rat liver sinusoidal endothelial cells from Kupffer cells in primary culture

Cited by 2 publications

References 12 publications

The Fibrin-Derived Peptide Bβ15-42 Attenuates Liver Damage in a Rat Model of Liver Ischemia/Reperfusion Injury

The Fibrin-Derived Peptide Bβ15-42 Attenuates Liver Damage in a Rat Model of Liver Ischemia/Reperfusion Injury

Cytokines, nitric oxide synthesis and liver regeneration

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