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PMID |
Sentence |
1 |
12934649
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In that study we suggested that EGCG could prevent cytokine-induced beta-cell destruction by down-regulation of nitric oxide synthase (NOS) through inhibition of NF-kappaB activation.
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2 |
15450943
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These results suggest that epicatechin inhibits the IL-1beta-induced iNOS expression by down-regulating NF-kappaB activation, and protecting beta-cells from IL-1beta.
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3 |
16177186
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Eight weeks later we measured TBARS and hydroperoxide-initiated chemiluminescence (QL) in liver as markers of oxidative stress, and activities of the antioxidant enzymes catalase, superoxide dismutase (SOD), and glutathione peroxidase, NF-kappaB activation by an electrophoretic mobility shift assay and expression of IkappaB kinases (IKKalpha and IKKbeta), the inhibitor IkappaB (IkappaBalpha and IkappaBbeta), and iNOS by Western blot.
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4 |
16177186
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Activation of NF-kappaB, induction of IKKalpha and iNOS protein levels, and increased degradation of IkappaBalpha were also observed in streptozotocin-treated rats.
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5 |
17462535
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This study establishes that AGE activate iNOS in VSMC through a ROS-sensitive, NF-kappaB-dependent mechanism involving ROS generation by a Nox1-based oxidase.
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6 |
17384130
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In this study we have investigated the effects of CBD on high glucose (HG)-induced, mitochondrial superoxide generation, NF-kappaB activation, nitrotyrosine formation, inducible nitric oxide synthase (iNOS) and adhesion molecules ICAM-1 and VCAM-1 expression, monocyte-endothelial adhesion, transendothelial migration of monocytes, and disruption of endothelial barrier function in human coronary artery endothelial cells (HCAECs).
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7 |
20713153
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CD44 stimulation activates the protein kinase C (PKC) family which in turn activates the transcriptional nuclear factor kappa B (NF-?B) responsible for the expression of the inflammation mediators such as tumor necrosis factor alpha (TNF-?), interleukin-6 (IL-6), interleukin-18 (IL-18), inducible nitric oxide synthase (iNOS), and matrix metalloproteinases (MMPs).
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8 |
9754830
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Transient transfection experiments with the 1.5-kb rat promoter region and 5' deletants of it showed that a distal region extending up to -1002 bp, and containing a distal and a proximal nuclear factor-kappaB (NF-kappaB) binding site, a gamma-interferon activated site (GAS) and two adjacent IFN-stimulated response elements (ISRE), is required for IL-1beta induction and IFN-gamma potentiation of iNOS activation.
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9 |
9754830
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Site-mutation analysis showed that both the distal and proximal NF-kappaB and GAS are necessary for IL-1beta-induced iNOS expression in RINm5F cells.
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10 |
9754830
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In these cells IFN-gamma potentiation is mostly mediated by GAS and ISRE, suggesting a role for the IFN-gamma-induced transcription factors Stat1alpha (which binds GAS) and IRF-1 (which binds ISRE), which may cooperate with NF-kappaB induced by IL-1beta for iNOS activation.
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11 |
9754830
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In primary beta cells both NF-kappaB binding sites are required for IL-1beta-induced iNOS promoter activation.
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12 |
11272138
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Inhibitors of NF-kappaB activation-the proteasome inhibitor MG-132 and the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + IFN-gamma-induced iNOS expression and nitric oxide production.
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13 |
11272138
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These results suggest that 1) NF-KB activation is required for dsRNA + IFN-gamma-induced iNOS expression, 2) PKR is not required for either dsRNA-induced NF-kappaB activation or dsRNA + IFN-y-induced iNOS expression by islets, and 3) PKR is not required for dsRNA + IFN-gamma-induced inhibition of glucose-stimulated insulin secretion by islets.
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