New method of delivering gene-altered Kupffer cells to rat liver: Studies in an ischemia-reperfusion model

2003 ◽  
Vol 124 (1) ◽  
pp. 172-183 ◽  
Author(s):  
Matthias Froh ◽  
Michael D. Wheeler ◽  
Olivia Smutney ◽  
Zhi Zhong ◽  
Blair U. Bradford ◽  
...  
Keyword(s):  
Rat Liver ◽  
Kupffer Cells ◽  
Ischemia Reperfusion ◽  
New Method

scholarly journals CD14 expression in Kupffer cells of ischemia-reperfusion injury after rat liver transplantation

2004 ◽  
Vol 12 (6) ◽  
pp. 1333
Author(s):  
Yong Peng ◽  
Jian-Ping Gong ◽  
Chang-An Liu ◽  
Sheng-Wei Li ◽  
Hai-Zhong Liu ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Rat Liver ◽  
Kupffer Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Liver Transplantation

Role of Kupffer cells in cold ischemia/reperfusion injury of rat liver

1995 ◽  
Vol 109 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Hiroshi Imamura ◽  
Fanny Sutto ◽  
Antoine Brault ◽  
Pierre-Michel Huet
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Kupffer Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cold Ischemia

scholarly journals Effects of blockade of Kupffer cells by gadolinium chloride on hepatobiliary function in cold ischemia-reperfusion injury of rat liver

Hepatology ◽  
1997 ◽  
Vol 26 (5) ◽  
pp. 1250-1257 ◽  
Author(s):  
M Kukan ◽  
K Vajdova ◽  
J Horecky ◽  
A Nagyova ◽  
H M Mehendale ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Kupffer Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Gadolinium Chloride ◽  
Cold Ischemia

Effect of taurine on IRAK4 and NF-kappa B in Kupffer cells from rat liver grafts after ischemia-reperfusion injury

2012 ◽  
Vol 204 (3) ◽  
pp. 389-395 ◽  
Author(s):  
Ke Sun ◽  
Yong Chen ◽  
Shao-yong Liang ◽  
Zuo-jing Liu ◽  
Wang-yang Liao ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Kupffer Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nf Kappa B

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.

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