Kupffer cells play an important role in the cytokine production and activation of nuclear factors of liver grafts from non-heart-beating donors

Oikawa, K; Ohkohchi, Nobuhiro; Sato, Masahide; Masamume, Atsuschi; Satoh, Susumu

doi:10.1111/j.1432-2277.2002.tb00188.x

Cited by 13 publications

(14 citation statements)

References 42 publications

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“…Similar results have been previously described [15,17,38]. Previous studies have also reported reduced amounts of TxB 2 release after Kupffer cell depletion in the setting of isolated liver perfusion and transplantation [50,51]. Our results demonstrated, however, that the elimination of Kupffer cells did not reduce TxB 2 release, but rather increased it.…”

Section: Discussioncontrasting

confidence: 50%

Role of Preferential Cyclooxygenase-2 Inhibition by Meloxicam in Ischemia/Reperfusion Injury of the Rat Liver

et al. 2014

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Background: Ischemia/reperfusion injury (IRI) is one of the major clinical problems in liver and transplant surgery. Livers subjected to warm ischemia in vivo often show a severe dysfunction and the release of numerous inflammatory cytokines and arachidonic acid metabolites. Cyclooxygenase (COX)-2 is the inducible isoform of an intracellular enzyme that converts arachidonic acid into prostaglandins. The aim of the study was to evaluate the effect of COX-2 inhibition and the role of Kupffer cells in IRI of the liver. Methods: Male Wistar rats [250- 280 g body weight (BW)] were anesthetized and subjected to 30-min warm ischemia of the liver (Pringle's maneuver) and 60-min reperfusion after median laparotomy. The I/R group received no additional treatment. In the COX-2 inhibitor (COX-2I) group, the animals received 1 mg/kg BW meloxicam prior to operation. Gadolinium chloride (GdCl₃) (10 mg/kg BW) was given 24 h prior to operation in the GdCl₃ and GdCl₃ + COX-2I groups for the selective depletion of Kupffer cells. The GdCl₃ + COX-2I group received both GdCl₃ and meloxicam treatment prior to operation. Blood and liver samples were obtained at the end of the experiments for further investigations. Results: After 30 min of warm ischemia in vivo, severe hepatocellular damage was observed in the I/R group. These impairments could be significantly prevented by the selective COX-2 inhibition and the depletion of Kupffer cells. Alanine aminotransferase was significantly reduced upon meloxicam and GdCl₃ treatment compared to the I/R group: I/R, 3,240 ± 1,262 U/l versus COX-2I, 973 ± 649 U/l, p < 0.001; I/R versus GdCl₃, 1,611 ± 600 U/l, p < 0.05, and I/R versus GdCl₃ + COX-2I, 1,511 ± 575 U/l, p < 0.01. Plasma levels of tumor necrosis factor alpha (TNF-α) were significantly reduced in the COX-2I treatment group compared to I/R (3.5 ± 1.5 vs. 16.3 ± 11.7 pg/ml, respectively; p < 0.05). Similarly, the amount of TxB₂, a marker for COX-2 metabolism, was significantly reduced in the meloxicam treatment groups compared to the I/R group: I/R, 22,500 ± 5,210 pg/ml versus COX-2I, 1,822 ± 938 pg/ml, p < 0.001, and I/R versus GdCl₃ + COX-2I, 1,530 ± 907 pg/ml, p < 0.001. All values are given as mean ± SD (n = 6). Conclusion: These results suggest that the inhibition of COX-2 suppressed the initiation of an inflammatory cascade by attenuating the release of TNF-α, which is an initiator of the inflammatory reaction in hepatic IRI. Therefore, we conclude that preferential inhibition of COX-2 is a possible therapeutic approach against warm IRI of the liver.

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Section: Discussioncontrasting

confidence: 50%

Role of Preferential Cyclooxygenase-2 Inhibition by Meloxicam in Ischemia/Reperfusion Injury of the Rat Liver

et al. 2014

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“…During the process, the injury of vascular endothelial cells and activation of the Kupffer cells induce the release of endotoxin and cytokines, produces massive iNOS, and then iNOS-induced NO damages the histiocytes [4] . In addition, lack of ATP in hepatic cells brings intracellular calcium overload, activates calcium dependent protease, and then produces xanthione oxidase.…”

Section: Effect Of Preservation Solution On No Expressionmentioning

confidence: 99%

Comparative study on the effects of self-made liver preservation solution on secretion of ICAM-1 and NO in rats

Wang

Dai

et al. 2008

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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In order to study the effect of self-made liver preservation solution on liver preservation by comparing with UW solution and HC-A solution, the self-made liver preservation solution (SM) and perfusion solution were prepared under the aseptic conditions. The isolated non-circulated perfusion rat liver model was established. According to the different preservation solutions, the rats were randomly divided into UW group, SM group and HC-A group. The three groups were divided into 6 subgroups according to the preservation duration (n=6 in each group). The transferase in liver perfusion solution and intercellular adhesion molecule-1 (ICAM-1) and nitric oxide (NO) in liver tissues were determined at 2, 8 and 24 h respectively. The results showed that the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) had no significant difference between SM group and UW group, but significantly lower than in HC-A group. The levels of ICAM-1 and NO were increased simultaneously in SM group and UW group (P>0.05), but there was significant difference as compared with HC-A group (P<0.05). At the same time point, the level of ICAM-1 was higher in SM group than in UW group, but NO was lower. The preservation effect of SM solution is the same as UW solution, but better than HC-A solution.

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“…It could result in excessive intracellular calcium [20], increasing free oxygen radicals in activated neutrophils and Kupffer cells and apoptosis in liver parenchymal cells [21,22]. Using proteomics technology, Hirsch et al [23] identified 1559 proteins in an HIRI model and found that IR caused certain inflammation-related proteins, such as calgranulin, C3, myeloperoxidase, copper/zinc superoxide dismutase, and hydrogen peroxide, to be up-regulated.…”

Section: Discussionmentioning

confidence: 96%

Hepatocellular Protein Profiles After Hepatic Ischemia/Reperfusion Injury With or Without Octreotide Preconditioning in a Rabbit Model

Yang

Sun

Guan

et al. 2014

Transplantation Proceedings

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Hepatic ischemic/reperfusion injury (HIRI) is a major complication of liver resection and transplantation. Octreotide, a somatostatin analogue, has been used to treat hepatic fibrosis and portal hypertension; however, its function against HIRI remains unclear. To elucidate the effect of octreotide in HIRI, we investigated the hepatocellular protein profiles in response to octreotide preconditioning in a rabbit model by using proteomic analysis. Twenty-four rabbits were divided into 3 groups: the sham operative group (control), the ischemia/reperfusion group (IR), and the ischemia/reperfusion + octreotide group (IR+Oct). They were subjected to 30 minutes of normothermic ischemia followed by 120 minutes of reperfusion by using Pringle's maneuver method. Proteomic studies were then performed to compare the protein profiles of their left liver lobe. A total of 16 differential proteins were successfully identified. These findings suggest that octreotide might exert an effect against HIRI through up-regulating the expression of the anti-injury substances, such as heat-shock proteins 70 and 27 (confirmed by using Western blot analysis); significantly raising the phosphatidylethanolamine-binding protein that alleviates IR-related apoptosis; and down-regulating mitochondrial metabolic enzymes such as NADH2 dehydrogenase and triosephosphate isomerase.

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Kupffer cells play an important role in the cytokine production and activation of nuclear factors of liver grafts from non-heart-beating donors

Cited by 13 publications

References 42 publications

Role of Preferential Cyclooxygenase-2 Inhibition by Meloxicam in Ischemia/Reperfusion Injury of the Rat Liver

Role of Preferential Cyclooxygenase-2 Inhibition by Meloxicam in Ischemia/Reperfusion Injury of the Rat Liver

Comparative study on the effects of self-made liver preservation solution on secretion of ICAM-1 and NO in rats

Hepatocellular Protein Profiles After Hepatic Ischemia/Reperfusion Injury With or Without Octreotide Preconditioning in a Rabbit Model

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