INT68651
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
RESULTS: Sevoflurane inhibited activation of the transcription factor AP-1. | |||||||||||||||
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Aspirin and aspirin-like salicylates inhibited the activation of AP-1 in the same dose range as seen for the inhibition of tumor promoter-induced transformation. | |||||||||||||||
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Overexpression of ICER in cultured spinal cord neurons results in the repression of the c-fos and c-jun promoters induced by forskolin and glutamate. | |||||||||||||||
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The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1. | |||||||||||||||
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CONCLUSION: Morphine inhibits activator protein 1 activation by a mu opioid receptor pathway coupled to nitric oxide as second messenger. | |||||||||||||||
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Treatment of melanoma cells with capsaicin inhibited activation of constitutive and IL-1beta-induced NF-kappaB, but not AP-1, leading to inhibition of IL-8 expression. | |||||||||||||||
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It achieved this by affecting phosphorylation of JNK and p38 MAPKs and consequently inhibiting c-jun and junD activation. | |||||||||||||||
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Inhibitory effects of curcumin and capsaicin on phorbol ester-induced activation of eukaryotic transcription factors, NF-kappaB and AP-1. | |||||||||||||||
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Based on these findings, it is likely that curcumin and capsaicin exert anti-tumor promotional effects through suppression of the tumor promoter-induced activation of transcription factors, NF-kappaB and AP-1. | |||||||||||||||
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Likewise, both compounds inhibited NF-kappaB and AP-1 activation in cultured human promyelocytic leukemia (HL-60) cells stimulated with TPA. | |||||||||||||||
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This resulted in the reduced accumulation of phosphorylated c-Jun and activation protein-1 DNA binding activity, and of activation protein-1-mediated inflammatory responses in OA chondrocytes. | |||||||||||||||
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