Vanillin suppresses Kupffer cell-related colloidal carbon-induced respiratory burst activity in isolated perfused rat liver: anti-inflammatory implications

2012 ◽  
Vol 3 (12) ◽  
pp. 1319 ◽  
Author(s):  
José E. Galgani ◽  
Bárbara Núñez ◽  
Luis A. Videla
Keyword(s):  
Rat Liver ◽  
Kupffer Cell ◽  
Respiratory Burst ◽  
Burst Activity ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Respiratory Burst Activity ◽  
Colloidal Carbon ◽  
Anti Inflammatory

Dose-dependent effects of acute lindane treatment on Kupffer cell function assessed in the isolated perfused rat liver

Xenobiotica ◽  
1997 ◽  
Vol 27 (7) ◽  
pp. 747-757 ◽  
Author(s):  
L. A. VIDELA* ◽  
P. TRONCOSO ◽  
A. C. M. ARISI ◽  
V. B. C. JUNQUEIRA
Keyword(s):  
Rat Liver ◽  
Kupffer Cell ◽  
Cell Function ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Dose Dependent

scholarly journals Time course study of the influence of acute iron overload on kupffer cell functioning and hepatotoxicity assessed in the isolated perfused rat liver

Hepatology ◽  
1998 ◽  
Vol 27 (5) ◽  
pp. 1311-1316 ◽  
Author(s):  
Gladys Tapia ◽  
Pilar Troncoso ◽  
Monica Galleano ◽  
Virginia Fernandez ◽  
Susana Puntarulo ◽  
...  
Keyword(s):  
Iron Overload ◽  
Rat Liver ◽  
Kupffer Cell ◽  
Time Course ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Time Course Study

scholarly journals Thyroid Hormone-Induced Cytosol-to-Nuclear Translocation of Rat Liver Nrf2 Is Dependent on Kupffer Cell Functioning

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Luis A. Videla ◽  
Pamela Cornejo ◽  
Pamela Romanque ◽  
Catherine Santibáñez ◽  
Iván Castillo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Kupffer Cell ◽  
Respiratory Burst ◽  
Oxidase Inhibitor ◽  
Burst Activity ◽  
Oxygen Species ◽  
Respiratory Burst Activity ◽  
Nadph Oxidase Inhibitor ◽  
Nrf2 Activation

L-3,3′,5-triiodothyronine (T3) administration upregulates nuclear factor-E2-related factor 2 (Nrf2) in rat liver, which is redox-sensitive transcription factor mediating cytoprotection. In this work, we studied the role of Kupffer cell respiratory burst activity, a process related to reactive oxygen species generation and liver homeostasis, in Nrf2 activation using the macrophage inactivator gadolinium chloride (GdCl3; 10 mg/kg i.v. 72 h before T3[0.1 mg/kg i.p.]) or NADPH oxidase inhibitor apocynin (1.5 mmol/L added to the drinking water for 7 days before T3), and determinations were performed 2 h after T3. T3increased nuclear/cytosolic Nrf2 content ratio and levels of heme oxygenase 1 (HO-1), catalytic subunit of glutamate cysteine ligase, and thioredoxin (Western blot) over control values, proteins whose gene transcription is induced by Nrf2. These changes were suppressed by GdCl3treatment prior to T3, an agent-eliciting Kupffer-cell depletion, inhibition of colloidal carbon phagocytosis, and the associated respiratory burst activity, with enhancement in nuclear inhibitor of Nrf2 kelch-like ECH-associated protein 1 (Keap1)/Nrf2 content ratios suggesting Nrf2 degradation. Under these conditions, T3-induced tumor necrosis factor-α(TNF-α) response was eliminated by previous GdCl3administration. Similar to GdCl3, apocynin given before T3significantly reduced liver Nrf2 activation and HO-1 expression, a NADPH oxidase inhibitor eliciting abolishment of colloidal carbon-induced respiratory burst activity without altering carbon phagocytosis. It is concluded that Kupffer cell functioning is essential for upregulation of liver Nrf2-signaling pathway by T3. This contention is supported by suppression of the respiratory burst activity of Kupffer cells and the associated reactive oxygen species production by GdCl3or apocynin given prior to T3, thus hindering Nrf2 activation.

scholarly journals A new method to monitor Kupffer-cell function continuously in the perfused rat liver. Dissociation of glycogenolysis from particle phagocytosis

1990 ◽  
Vol 266 (1) ◽  
pp. 141-147 ◽  
Author(s):  
K B Cowper ◽  
R T Currin ◽  
T L Dawson ◽  
K A Lindert ◽  
J J Lemasters ◽  
...  
Keyword(s):  
Rat Liver ◽  
Kupffer Cell ◽  
Kupffer Cells ◽  
Cell Function ◽  
New Method ◽  
Carbon Uptake ◽  
Prostaglandin D2 ◽  
Perfused Rat Liver ◽  
Colloidal Carbon ◽  
Parenchymal Cells

In order to study particle phagocytosis and glycogenolysis simultaneously, this study was designed to develop a direct-read-out method to monitor Kupffer-cell function continuously, based on the uptake of colloidal carbon by the isolated perfused rat liver. Livers were perfused for 20 min with Krebs-Henseleit buffer saturated with O2/CO2 (19:1). Colloidal carbon (1-2 mg/ml) was added to the buffer, and absorbance of carbon was monitored continuously at 623 nm in the effluent perfusate. Since colloidal-carbon uptake was proportional to A623, rates of uptake were determined from the influent minus effluent concentration difference, the flow rate and the liver wet weight. Rates of colloidal-carbon uptake were 50-200 mg/h per g and were proportional to the concentration of carbon infused. Data from light-microscopy and cell-separation studies demonstrated that carbon was taken up exclusively by non-parenchymal cells and predominantly by Kupffer cells. Further, the amount of colloidal carbon detected histologically in non-parenchymal cells increased as the concentration of colloidal carbon in the perfusate was elevated. When Kupffer cells were activated or inhibited by treatment with endotoxin or methyl palmitate, carbon uptake was increased or decreased respectively. Taken together, these results indicate that Kupffer-cell function can be monitored continuously in a living organ. This new method was utilized to compare the time course of phagocytosis of carbon by Kupffer cells and carbohydrate output by parenchymal cells. Carbohydrate output increased rapidly by 69 +/- 9 mumol per g within 2-4 min after addition of carbon and returned to basal values within 12-16 min. However, carbon uptake by the liver did not reach maximal rates until about 15 min. Infusion of a cyclo-oxygenase inhibitor, aspirin (10 mM), caused a progressive decrease in carbohydrate output and blocked the stimulation by carbon completely. Aspirin neither altered rates of carbon uptake nor prevented stimulation of carbohydrate release by addition of N2-saturated buffer. The data from these experiments are consistent with the hypothesis that output of mediators by Kupffer cells, presumably prostaglandin D2 and E2, occurs transiently as Kupffer cells begin to phagocytose foreign particles in the intact organ, a process which continues at high rates for hours.

A Comparison of Plasminogen Activators Derived from Rat Plasma, Primary Rat Hepatocytes and Isolated Perfused Rat Liver

1982 ◽  
Vol 47 (02) ◽  
pp. 166-172 ◽  
Author(s):  
Yoav Sharoni ◽  
Maria C Topal ◽  
Patricia R Tuttle ◽  
Henry Berger
Keyword(s):  
Rat Liver ◽  
Isoelectric Point ◽  
Rat Hepatocytes ◽  
Cell Types ◽  
Plasminogen Activators ◽  
Rat Plasma ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Molecular Weights ◽  
Physiological Relevance

SummaryOf the two cell types it was possible to culture from the dissociated rat liver, hepatocytes and Kupffer cells, only the former were fibrinolytically active. Rat hepatocytes during the first 24 hr in culture secreted two plasminogen activators with molecular weights identical to those found in rat plasma, an 80,000-dalton form (PA-80) and a 45,000-dalton form (PA-45). Partially purified preparations of plasminogen activators from both sources were subjected to isoelectric focusing (IEF) to compare characteristics further. There were three distinct peaks of PA-45 in each preparation with isoelectric points of 7.1, 7.2 and 7.4; all electrophoretic forms had the same low affinity to fibrin. PA-80 from both sources displayed similar IEF profiles with forms ranging from pH values of 7 to 8, all with the same high affinity to fibrin. The major form of PA-80 in the plasma preparation had an isoelectric point of 7.9 whereas that in the hepatocyte preparation had an isoelectric point of 7.6. The isolated perfused rat liver was also shown to produce both PA-80 and PA-45 emphasizing the physiological relevance of the findings with hepatocytes. It is concluded that in the rat hepatocytes contribute to the plasma profile with regard to the plasminogen activator content.

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