INT71879
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In the present study, topical application of capsaicin onto dorsal skin of female ICR mice strongly suppressed phorbol ester-stimulated activation of NF-kappaB via blockade of IkappaB-alpha degradation with subsequent inhibition of nuclear translocation of the functionally active NF-kappaB subunit, p65. | |||||||||||||||
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In further studies, NNU-hdpa was found to significantly inhibit the productions of PGE(2) and LTB(4) in LPS-challenged RAW 264.7, which is parallel to its prevention of the nuclear translocation of the NF-kappaB p50 and p65 subunits. | |||||||||||||||
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We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. | |||||||||||||||
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PEA prevented IkB-alpha degradation and p65 NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral hyperalgesia. | |||||||||||||||
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Since bee venom and melittin delay and reduce nuclear translocation of the p50 subunit of NF? | |||||||||||||||
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ME10092 dose-dependently inhibited LPS-induced nuclear translocation of NF-kappaB, transcription of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). | |||||||||||||||
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Mice subjected to renal IR under isoflurane anesthesia also showed a reduction in inflammation evidenced by a reduced renal influx of neutrophils and macrophages, reduced ICAM-1 expression, less upregulation of proinflammatory mRNAs (TNF-alpha, ICAM-1, KC, and IL-1beta) as well as reduced nuclear translocation of NF-kappaB 24 h after renal IR injury. | |||||||||||||||
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Mice subjected to renal IR under isoflurane anesthesia also showed a reduction in inflammation evidenced by a reduced renal influx of neutrophils and macrophages, reduced ICAM-1 expression, less upregulation of proinflammatory mRNAs (TNF-alpha, ICAM-1, KC, and IL-1beta) as well as reduced nuclear translocation of NF-kappaB 24 h after renal IR injury. | |||||||||||||||
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We previously reported that depletion of glutathione in murine hepatocytes by diethylmaleate (DEM) or acetaminophen (APAP) leads to oxidative stress-dependent necrosis and sensitizes to tumor necrosis factor (TNF)-induced apoptosis in an oxidative stress-independent fashion, which could not be explained by interference with nuclear factor kappaB (NF-kappaB) nuclear translocation. | |||||||||||||||
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Central administration of palmitoylethanolamide reduces hyperalgesia in mice via inhibition of NF-kappaB nuclear signalling in dorsal root ganglia. | |||||||||||||||
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Furthermore, MEXS inhibited nuclear factor kappa B (NF-kappaB) DNA binding activity and the translocation of NF-kappaB to the nucleus by blocking the degradation of inhibitor of kappa B-alpha (IkappaB-alpha). | |||||||||||||||
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PEA prevented IkB-alpha degradation and NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral inflammation. | |||||||||||||||
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Therefore, we hypothesized that excessive IL-6 expression decreased LPS-induced neutrophil emigration in p50-deficient mice. | |||||||||||||||
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Moreover, the translocation of NF-kappaB in nucleus resulted from Ang II was reduced by treatment with U0126. | |||||||||||||||
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In support of this concept, we found, using inhibitors of Jun kinase and NF-kappaB p50 nuclear localization, that COX-2 gene transcription was completely dependent on phospho-c-Jun plus p50 at 6 h after LPS treatment but was only partially dependent on the combination of these factors at later treatment times. | |||||||||||||||
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In support of this concept, we found, using inhibitors of Jun kinase and NF-kappaB p50 nuclear localization, that COX-2 gene transcription was completely dependent on phospho-c-Jun plus p50 at 6 h after LPS treatment but was only partially dependent on the combination of these factors at later treatment times. | |||||||||||||||
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In this study, we show that reducing ERK5 levels with a specific small hairpin RNA 5 (shERK5) reduced cell viability, sensitized cells to death receptor-induced apoptosis, and blocked the palliative effects of phorbol ester in anti-Fas Ab-treated cells. shERK5 decreased nuclear accumulation of the NF-kappaB p65 subunit, and conversely, ectopic activation of ERK5 led to constitutive nuclear localization of p65 and increased its ability to trans activate specific reporter genes. | |||||||||||||||
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Furthermore, our data also demonstrated that the translocation of NF-kappaB activated by LPS into the nucleus was suppressed by menthone, and I-kappaB and beta-transducin repeat containing protein (beta-TrCP) were both involved in this suppression. | |||||||||||||||
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All three salicylates inhibited the diabetes-induced translocation of p50 (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections. | |||||||||||||||
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Certain NSAIDs, such as flurbiprofen and indomethacin, inhibit the nuclear translocation of the transcription factor NF-kB. | |||||||||||||||
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