INT65054
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Moreover, this compound reduces the increased NF-kappaB binding activity, which occurs in these degenerative conditions. | |||||||||||||||
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Moreover, activation of NF-kappaB by amyloid-derived peptides was greatly impaired by acetaminophen pre-treatment in hippocampal cells. | |||||||||||||||
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Pregabalin and gabapentin inhibit substance P-induced NF-kappaB activation in neuroblastoma and glioma cells. | |||||||||||||||
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Pregabalin and gabapentin decreased substance P-induced NF-kappaB activation in these cells. | |||||||||||||||
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In this study, we investigated their actions on substance P-induced NF-kappaB activation in human neuroblastoma and rat glioma cells. | |||||||||||||||
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These drugs also inhibited NF-kappaB activation in rat spinal dorsal root ganglia cells pre-treated in vitro with substance P. | |||||||||||||||
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Our results support NF-kappaB activation in EAN during the induction stage as well as in the disease remission. | |||||||||||||||
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These findings indicate that excess mechanical stress increases NF-kappaB activation in the TMJ and suggest that active NF-kappaB is involved in the progression of TMJ inflammation. | |||||||||||||||
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NF-kappaB activation and iNOS expression in the synovial membrane of rat temporomandibular joints after induced synovitis. | |||||||||||||||
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These results suggest that atorvastatin may be a novel and promising candidate for future treatment or prophylaxis of migraine via attenuating activation of NF-kappaB in trigeminal nucleus caudalis. | |||||||||||||||
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Thus, this study aims to explore whether atorvastatin attenuates NF-kappaB activation in trigeminal nucleus caudalis in a nitroglycerin-induced migraine model. | |||||||||||||||
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CONCLUSION: The activation of NF-kappaB and its downstream inflammatory mediators may be involved in the regulation of neuropathic pain.
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The DNA binding activity of NF kappa B was increased compared with the hypoxic group. | |||||||||||||||
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CONCLUSION: The activation of NF-kappaB pathway may contribute to neuropathic pain in CCI rats. | |||||||||||||||
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Different criteria suggest that the observed effects are mediated at least in part through inhibition of NF-kB activation: R-flurbiprofen inhibited i) LPS-induced NF-kB DNA binding activity in RAW 264.7 macrophages, ii) translocation of the p65 subunit of NF-kB into the nucleus of these cells, and iii) zymosan-induced NF-kB-dependent gene transcription in the inflamed paw and spinal cord of rats. | |||||||||||||||
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Inhibition of NF-kappaB and AP-1 activation by R- and S-flurbiprofen. | |||||||||||||||
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Neuroprotection by aspirin and sodium salicylate through blockade of NF-kappaB activation. | |||||||||||||||
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In rats pretreated with EcN, a significant downregulation of mRNA and protein expression for IL-1beta, COX-2 and PPARgamma and increased expression of HSP70 without major change in activation of NFkappaB were observed. | |||||||||||||||
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Activation of NF-kappaB in brain areas was detected by means of both the immunohistochemical technique and the Western blot analysis. | |||||||||||||||
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In the present study, we sought to elucidate whether NF-kappaB activation might have a role in the determinism of migraine attacks also at the neuronal level. | |||||||||||||||
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