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Puslapis 1 nuo 16 rezultatus
Inhibition of MCP-1 and MIP-2 chemokines in murine trichinellosis: effect of the anti-inflammatory compound L-mimosine.
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Mimosine is a plant amino-acid which has been reported to block DNA replication in mammalian cells and to arrest cell reversibly towards the end of the G1 phase or at the beginning of the S phase. In this study, 42 mice were infected with T. spiralis a nematode parasite, and treated with the
Inhibition of MCP-1 and MIP-2 transcription and translation by mimosine in muscle tissue infected with the parasite Trichinella spiralis.
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Mimosine is a non-toxic plant aminoacid which is an effective inhibitor of DNA replication by acting at the S-phase. In this study we infected mice with T. spiralis, a nematode parasite, and studied the inflammatory response through the determination of MIP-2, a C-X-C chemokine and MCP-1, a C-C
A spectrum of antibody (IgG. IgG1, IgM) response in mice infected with trichinella spiralis treated with L-mimosine.
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The purpose of this study was to demonstrate the anti-inflammatory effects of L-mimosine on chronic inflammation, by investigating its effect on the immunological response of BALB/c mice infected with the nematode parasite Trichinella spiralis. Specific anti-parasite immunoglobulins (IgG, IgG1 and
Effect of the compound L-mimosine in an in vivo model of chronic granuloma formation induced by potassium permanganate (KMNO4).
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The plant amino acid L-mimosine has recently been suggested to inhibit cells at a regulatory step in late G1 phase before establishment of active DNA replication forks. In addition, L-mimosine is an extremely effective inhibitor of DNA replication in chromosomes of mammalian nuclei. In this work,
Suppressive effects of Mimosa pudica (L.) constituents on the production of LPS-induced pro-inflammatory mediators.
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The present study deals with the isolation of fourteen compounds from the active ethyl acetate (MPE) extract of M. pudica (L.) whole plant and their subsequent evaluation for the nitric oxide (NO), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1ß) inhibitory activities in
Response of ADA and its isoenzymes in mice infected by Trichinella spiralis and treated with mimosine.
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Infections caused by the nematode Trichinella spiralis (T. spiralis) are characterized by an inflammatory response in the host. The aim of this study was to identify and evaluate markers for monitoring mice infected with T. spiralis and treated with or without mimosine. The markers that have been
L-mimosine and dimethyloxaloylglycine decrease plasminogen activation in periodontal fibroblasts.
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BACKGROUND
The use of prolyl hydroxylase inhibitors such as l-mimosine (L-MIM) and dimethyloxaloylglycine (DMOG) to improve angiogenesis is a new approach for periodontal regeneration. In addition to exhibiting pro-angiogenic effects, prolyl hydroxylase inhibitors can modulate the plasminogen
The Influence of Pro-Inflammatory Factors on Sclerostin and Dickkopf-1 Production in Human Dental Pulp Cells Under Hypoxic Conditions.
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Sclerostin (Sost) and dickkopf (Dkk)-1 are inhibitors of the Wnt signaling pathway that plays a role in regenerative processes. Hypoxia-based strategies are used for regenerative approaches, but the influence of hypoxia on Sost and Dkk-1 production in a pro-inflammatory environment is unclear. The
L-mimosine increases the production of vascular endothelial growth factor in human tooth slice organ culture model.
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OBJECTIVE
To assess the pro-angiogenic and pro-inflammatory capacity of the dentine-pulp complex in response to the prolyl hydroxylase inhibitor L-mimosine in a tooth slice organ culture model.
METHODS
Human teeth were sectioned transversely into 600-μm-thick slices and cultured in medium
Metal self-assembly mimosine peptides with enhanced antimicrobial activity: towards a new generation of multitasking chelating agents.
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Mimosine is a non-protein amino acid with various properties, such as antibacterial, anti-inflammatory, anti-cancer and anti-virus among others. Due to its structural similarity with deferiprone (DFP), mimosine is a potential excellent metal chelator. In the present work, we combine experimental and
Iron-mediated H2O2 production as a mechanism for cell type-specific inhibition of tumor necrosis factor alpha-induced but not interleukin-1beta-induced IkappaB kinase complex/nuclear factor-kappaB activation.
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Coordinated and specific regulation of tumor necrosis factor (TNF) and interleukin (IL)-1 signaling pathways and how and whether they are modified by different agents are key events for proper immune responses. The IkappaB kinase complex (IKK)/NF-kappaB and JNK/AP-1 pathways are central mediators of
Prolyl hydroxylase 2 (PHD2) inhibition protects human renal epithelial cells and mice kidney from hypoxia injury.
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Prolyl hydroxylase domain protein 2 (PHD2) is a key oxygen sensor, setting low steady-state level of hypoxia-inducible factor-α (HIF-α). Here, we showed that treatment of cobalt chloride (CoCl2), a hypoxia mimic, in HK-2 tubular epithelial cells induced PHD2 and HIF-1/2α expression as well as cell
Hypoxia and upregulation of hypoxia-inducible factor 1{alpha} stimulate venous thrombus recanalization.
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OBJECTIVE
Angiogenic factors are expressed within thrombus during resolution, but the primary stimulus for neovascularization is unknown. Our aims were to determine whether (1) hypoxia and hypoxia-inducible factor 1α (HIF1α) are induced in resolving thrombus, (2) this stimulates angiogenic factor
Immune-related chemotactic factors were found in acute coronary syndromes by bioinformatics.
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DNA microarray data for thrombus-related leukocyte from patients with acute coronary syndrome (ACS) was analyzed to acquire key genes associated with ACS. Microarray data set GSE19339, including four ACS patients' samples and four normal samples, were downloaded from Gene Expression Omnibus
Inhibition of prolyl hydroxylase domain proteins selectively enhances venous thrombus neovascularisation.
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Hypoxia within acute venous thrombi is thought to drive resolution through stabilisation of hypoxia inducible factor 1 alpha (HIF1α). Prolyl hydroxylase domain (PHD) isoforms are critical regulators of HIF1α stability. Non-selective inhibition of PHD isoforms with l-mimosine has been shown to
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