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concanavalin a/nekrosis
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Pentoxifylline prevents concanavalin A-induced hepatitis by reducing tumor necrosis factor alpha levels and inhibiting adhesion of T lymphocytes to extracellular matrix.
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OBJECTIVE
Concanavalin A activates T lymphocytes and causes T cell-mediated hepatic injury in mice. Tumor necrosis factor alpha is a critical mediator in this experimental model. T-cell-mediated liver injury involves the migration of immune cells, notably CD4+ T lymphocytes, into liver tissue.
Analysis of Arg-Gly-Asp mimetics and soluble receptor of tumour necrosis factor as therapeutic modalities for concanavalin A induced hepatitis in mice.
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It has been shown that synthetic non-peptidic analogues of Arg-Gly-Asp, a major cell adhesive ligand of extracellular matrix, prevented an increase in serum aminotransferase activity, as a manifestation of concanavalin A induced liver damage in mice. This study examined the effects of an
Neutralization of bovine concanavalin-A T cell supernatant-mediated anti-Cowdria ruminantium activity with antibodies specific to interferon gamma but not to tumor necrosis factor.
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In an earlier study we demonstrated that Concanavalin-A stimulated bovine T cell supernatants inhibited the growth of Cowdria ruminantium in bovine endothelial cells in vitro. An investigation was conducted to identify the cytokines which were responsible for this growth inhibition. Addition of
Rutin inhibits nitric oxide and tumor necrosis factor-alpha production in lipopolysaccharide and concanavalin-a stimulated macrophages.
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The effect of rutin, a flavonoid present in onions, apples, tea and red wine, on the production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) was analyzed using in vitro as well as in vivo systems. The level of nitrite in lipopolysaccharide (LPS) stimulated BALB/c mice (88.21
Cooperative stimulatory effects of tumor necrosis factor and granulocyte-macrophage colony-stimulating factor on the particular respiratory burst activity in human neutrophils: synergistic priming effect on concanavalin A-induced response, no interactive priming effect on the chemotactic peptide-induced response and additive triggering effect.
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Tumor necrosis factor (TNF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) rapidly primed human neutrophils for enhanced superoxide (O2-) release, and membrane depolarization stimulated by chemotactic peptide
Selective inhibition of tumor necrosis factor-α converting enzyme attenuates liver toxicity in a murine model of concanavalin A induced auto-immune hepatitis.
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Emerging evidence suggest that tumor necrosis factor (TNF)-α plays a major role in pathogenesis of auto-immune hepatitis (AIH) induced liver injury. Blockade of TNF-α synthesis or bio-activity protects against experimental AIH. TNF-α converting enzyme (TACE) is a member of the ADAM (a disintegrin
Midzonal necrosis of the liver after concanavalin A-injection.
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Concanavalin A (Con A) can induce an immune-mediated hepatitis. Since direct evidence of immune mechanism for this hepatitis is lacking, we employed adoptive transfer to study the mechanism of Con A-induced hepatitis. Intravenous administration of Con A (20 mg/kg) to Balb/c mice was accompanied by
Antitumour activity of endotoxin, concanavalin A and poly I: C and their ability to elicit tumour necrosis factor, cytostatic factors, and interferon in vivo.
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Concanavalin A, endotoxin, poly I: C, and tumour necrosis serum (TNS) were compared for antitumour activity against Meth A sarcoma transplanted in syngeneic BALB/c mice and their capacity to induce tumour necrosis factor (TNF), heat-stable cytostatic factors, and heat-labile interferon in the blood
Ursodeoxycholic acid protects concanavalin A-induced mouse liver injury through inhibition of intrahepatic tumor necrosis factor-alpha and macrophage inflammatory protein-2 production.
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Ursodeoxycholic acid (UDCA) is widely used for the therapy of liver dysfunction. In this study, we investigated the protective effect of UDCA in concanavalin A-induced mouse liver injury. The treatment with UDCA at oral doses of 50 and 150 mg/kg at 2 h before concanavalin A injection significantly
Concanavalin A-induced liver cell damage: activation of intracellular pathways triggered by tumor necrosis factor in mice.
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OBJECTIVE
Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. Intracellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-kappaB translocation, or Jun
Increased tumour necrosis factor-alpha production, higher mannose receptor activity and ability to kill Candida by concanavalin-A-activated macrophages.
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In a previous study, our group verified that mice pretreated with concanavalin-A (Con-A) produced more tumour necrosis factor (TNF)-alpha and presented greater Candida clearance from the peritoneal cavity, liver and spleen, which yielded a higher survival rate than control animals. In this work, the
Echinacea purpurea Root Extract Increases Tumor Necrosis Factor Production by Concanavalin A-Activated Murine Splenocytes.
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Echinacea purpurea is a common herbal remedy used to treat a variety of illnesses, though its health benefits and effects on the immune system have not been fully elucidated. In this study, we investigated the effect of E. purpurea root extract on the survival of concanavalin A
Concanavalin A hepatotoxicity in mice: tumor necrosis factor-mediated organ failure independent of caspase-3-like protease activation.
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Several models of tumor necrosis factor (TNF)/TNF-receptor 1 (TNF-R1)-dependent liver injury in mice were investigated with respect to caspase-3-like protease activation representing a pivotal mechanism of apoptotic cell death. Injection of TNF or T-cell-activating agents (i.e., agonistic anti-CD3
Concanavalin A-induced T-cell-mediated hepatic injury in mice: the role of tumor necrosis factor.
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Concanavalin A activates T lymphocytes in vitro and causes T-cell-dependent hepatic injury in mice. T lymphocytes were previously identified as effector cells of concanavalin A-induced liver injury. Here we report that hepatic injury is characterized by apoptotic cell death. On concanavalin A
Methane-rich saline protects against concanavalin A-induced autoimmune hepatitis in mice through anti-inflammatory and anti-oxidative pathways.
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Methane is a common gas which has been reported to play a protective role in organ injury and presents an anti-inflammatory property. However, its effects on Concanavalin A (Con A)-induced autoimmune hepatitis (AIH) remain unknown. Thus, the aim of this study was to investigate the effects of
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