INT53949
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Twenty-five weeks after the initiation of NMBA treatment, we observed an elevation in COX mRNA and protein expression and prostaglandin E(2) production in NMBA-treated esophageal tissues compared with normal epithelium. | |||||||||||||||
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In this study, we characterized COX-mediated arachidonic acid metabolism in NMBA-induced rat esophageal tumorigenesis by measuring COX-1 and COX-2 expression and prostaglandin E(2) production. | |||||||||||||||
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In this study, we characterized COX-mediated arachidonic acid metabolism in NMBA-induced rat esophageal tumorigenesis by measuring COX-1 and COX-2 expression and prostaglandin E(2) production. | |||||||||||||||
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ONOO(-) generated by the interaction between exogenous administration of O(2)(*-) and endogenous *NO, or provided by direct injection of ONOO(-), activated the transcription factor NF-kappaB in paw tissues, enhancing expression of the inducible but not the constitutive cyclooxygenase enzyme (COX-2 and COX-1, respectively). | |||||||||||||||
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COX-2 is overexpressed in cancer cells and has become a major target for cancer preventive drugs. | |||||||||||||||
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Both drugs stimulated COX-2 expression in accordance to their capacity of inhibiting this enzymatic activity, driving to delay in the healing. | |||||||||||||||
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RESULTS: Time-course studies with use of both Western blot protein analysis and immunohistochemistry demonstrated a transient upregulation of COX-2 protein expression with peak levels eight to twelve hours after trauma and a return to near baseline level at eighteen hours. | |||||||||||||||
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Immunohistological studies showed that COX-2 protein expression was enhanced in neurons. | |||||||||||||||
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Mucosal PGE2 content was increased following IA treatment, with apparent expression of COX-2 mRNA in the stomach, and the increased PGE2 production was significantly suppressed by SC-560 and rofecoxib as well as indomethacin. | |||||||||||||||
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ONOO(-) generated by the interaction between exogenous administration of O(2)(*-) and endogenous *NO, or provided by direct injection of ONOO(-), activated the transcription factor NF-kappaB in paw tissues, enhancing expression of the inducible but not the constitutive cyclooxygenase enzyme (COX-2 and COX-1, respectively). | |||||||||||||||
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COX-2 protein expression was also highly elevated in comparison to healthy controls. | |||||||||||||||
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The inflammation in PHN induced COX-2 protein expression that was not affected by low-dose flosulide. | |||||||||||||||
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Additional experiments showed increased COX-2 mRNA expression in the renal medulla 60 min after ketoprofen administration, that was not significantly influenced by concomitant caffeine treatment. | |||||||||||||||
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On the other hand, new therapeutic indications have emerged as a result of the role played by COX-2 overexpression in cancer or Alzheimer's disease. | |||||||||||||||
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The inhibition of COX-1 up-regulates COX-2 expression, and this may be a key to NSAID-induced intestinal damage. | |||||||||||||||
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In neuroblastoma it has been shown that the majority of primary tumours and cell lines express high levels of COX-2, whereas normal adrenal medullas from children do not express COX-2. | |||||||||||||||
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The expression of COX-1 mRNA remained unchanged in all tissues examined. | |||||||||||||||
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Although COX-1 mRNA was expressed in the colon without much alteration during the test period, the expression of COX-2 was upregulated with a peak on day 3 and decreased thereafter. | |||||||||||||||
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I/R also increased the expression of COX-2, and this increase was suppressed by pretreatment with DPI. | |||||||||||||||
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Furthermore, COX-2 expression was significantly elevated with indomethacin and SC-560, explaining the source of augmented PGE(2) synthesis. | |||||||||||||||
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General Comments
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