Kupffer’s cells modulate neutrophile activity by superoxide anion and tumor necrosis factor–∂ in reperfusion injury of liver transplantation-mechanisms of radical generation and reperfusion injury after cold ischemia

Ohkohchi, Nobuhiro; Shibuya, H.; Tsukamoto, Shigeki; Sakurada, M; Oikawa, K; Terashima, Toru; Satoh, Susumu

doi:10.1016/s0041-1345(98)01902-2

Cited by 8 publications

(6 citation statements)

References 9 publications

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“…These leukocytes induce elevated oxygen consumption [22], release abundant proteases, and generate oxygen radicals [23]. Therefore, the release of elastase and reactive oxygen species from these leukocytes is considered to be the main cause of liver tissue injury [24,25]. In the present study, sivelestat significantly decreased the number of infiltrating leukocytes and also significantly reduced perfusion disturbance after hepatic I/R.…”

Section: Discussionsupporting

confidence: 54%

Prevention of Leukocyte Activation by the Neutrophil Elastase Inhibitor, Sivelestat, in the Hepatic Microcirculation After Ischemia-Reperfusion

Nakano

Kondo

Matsuo

et al. 2009

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 54%

Prevention of Leukocyte Activation by the Neutrophil Elastase Inhibitor, Sivelestat, in the Hepatic Microcirculation After Ischemia-Reperfusion

Nakano

Kondo

Matsuo

et al. 2009

Journal of Surgical Research

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“…Adhesion molecules mediate the initial attachment of neutrophils to the activated endothelium [54,55], which is a crucial event in initiation of liver I/R injury [55][56][57][58]. On reperfusion, TNF-α acts as a continuous stimulator for neutrophil infiltration in the liver, and it also up-regulates the production of chemokines, which may contribute to the up-regulation of cell adhesion molecules and neutrophil activation as well [57].…”

Section: Discussionmentioning

confidence: 99%

Pivotal Advance: Cannabinoid-2 receptor agonist HU-308 protects against hepatic ischemia/reperfusion injury by attenuating oxidative stress, inflammatory response, and apoptosis

Rajesh¹,

Pān²,

Mukhopadhyay³

et al. 2007

Journal of Leukocyte Biology

130

142

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In this study, we have investigated the role of the cannabinoid CB 2 (CB 2 ) receptor in an in vivo mouse model of hepatic ischemia/reperfusion (I/R) injury. In addition, we have assessed the role of the CB 2 receptor in TNF-α-induced ICAM-1 and VCAM-1 expression in human liver sinusoidal endothelial cells (HLSECs) and in the adhesion of human neutrophils to HLSECs in vitro. The potent CB 2 receptor agonist HU-308, given prior to the induction of I/R, significantly attenuated the extent of liver damage (measured by serum alanine aminotransferase and lactate dehydrogenase) and decreased serum and tissue TNF-α, MIP-1α, and MIP-2 levels, tissue lipid peroxidation, neutrophil infiltration, DNA fragmentation, and caspase 3 activity. The protective effect of HU-308 against liver damage was also preserved when given right after the ischemic episode. HU-308 also attenuated the TNF-α-induced ICAM-1 and VCAM-1 expression in HLSECs, which expressed CB 2 receptors, and the adhesion of human neutrophils to HLSECs in vitro. These findings suggest that selective CB 2 receptor agonists may represent a novel, protective strategy against I/R injury by attenuating oxidative stress, inflammatory response, and apoptosis.

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“…It is well established that liver I/R injury is dependent on PMN infiltration, Kupffer cell activation, and cytokine response (57)(58)(59)(60). Adhesion molecules mediate the initial attachment of neutrophils to the activated endothelium (58,61).…”

Section: Cbmentioning

confidence: 99%

Cannabinoid‐2 receptor mediates protection against hepatic ischemia/reperfusion injury

et al. 2007

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Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication that can follow liver surgery or transplantation. We have investigated the involvement of the endocannabinoid system in hepatic I/R injury using an in vivo mouse model. Here we report that I/R triggers several-fold increases in the hepatic levels of the endocannabinoids anandamide and 2-arachidonoylglycerol, which originate from hepatocytes, Kupffer, and endothelial cells. The I/R-induced increased tissue endocannabinoid levels positively correlate with the degree of hepatic damage and serum TNF-alpha, MIP-1alpha, and MIP-2 levels. Furthermore, a brief exposure of hepatocytes to various oxidants (H2O2 and peroxynitrite) or inflammatory stimuli (endotoxin and TNF-alpha) also increases endocannabinoid levels. Activation of CB2 cannabinoid receptors by JWH133 protects against I/R damage by decreasing inflammatory cell infiltration, tissue and serum TNF-alpha, MIP-1alpha and MIP-2 levels, tissue lipid peroxidation, and expression of adhesion molecule ICAM-1 in vivo. JWH133 also attenuates the TNF-alpha-induced ICAM-1 and VCAM-1 expression in human liver sinusoidal endothelial cells (HLSECs) and the adhesion of human neutrophils to HLSECs in vitro. Consistent with the protective role of CB2 receptor activation, CB2-/- mice develop increased I/R-induced tissue damage and proinflammatory phenotype. These findings suggest that oxidative/nitrosative stress and inflammatory stimuli may trigger endocannabinoid production, and indicate that targeting CB2 cannabinoid receptors may represent a novel protective strategy against I/R injury. We also demonstrate that CB2-/- mice have a normal hemodynamic profile.

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Kupffer’s cells modulate neutrophile activity by superoxide anion and tumor necrosis factor–∂ in reperfusion injury of liver transplantation-mechanisms of radical generation and reperfusion injury after cold ischemia

Cited by 8 publications

References 9 publications

Prevention of Leukocyte Activation by the Neutrophil Elastase Inhibitor, Sivelestat, in the Hepatic Microcirculation After Ischemia-Reperfusion

Prevention of Leukocyte Activation by the Neutrophil Elastase Inhibitor, Sivelestat, in the Hepatic Microcirculation After Ischemia-Reperfusion

Pivotal Advance: Cannabinoid-2 receptor agonist HU-308 protects against hepatic ischemia/reperfusion injury by attenuating oxidative stress, inflammatory response, and apoptosis

Cannabinoid‐2 receptor mediates protection against hepatic ischemia/reperfusion injury

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