INT7996
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In contrast, basal expression of lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia was not significantly altered by endotoxin. | |||||||||||||||
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Dexamethasone (1 mg/kg s.c. at -18 h and -1 h) attenuated the effect endotoxin on the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in all tissues investigated, but did not significantly influence expression of lipocalin prostaglandin D synthase mRNA in spinal cord and dorsal root ganglia. | |||||||||||||||
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PGD2 produced a dose-related inflammation-augmenting effect, whereas hydrocortisone and the PG synthesis inhibitors, paracetamol and mefenamic acid, induced attenuation of the peripheral oedema. | |||||||||||||||
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Prostaglandin (PG) D2 represented approximately 10% of the PGs produced in the lumen, irrespective of the presence or absence of luminal PGDS, suggesting that this protein is not involved in PGD2 biosynthesis. | |||||||||||||||
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Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats. | |||||||||||||||
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Prostaglandin D2(PGD2) is the most produced prostanoid in the CNS of mammals, and in behavioral experiments it has been implicated in the modulation of spinal nociception. | |||||||||||||||
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Prostaglandin D2(PGD2) is the most produced prostanoid in the CNS of mammals, and in behavioral experiments it has been implicated in the modulation of spinal nociception. | |||||||||||||||
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COX-2-mediated PGD2 synthesis regulates phosphatidylcholine biosynthesis in rat renal papillary tissue. | |||||||||||||||
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In contrast, basal expression of lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia was not significantly altered by endotoxin. | |||||||||||||||
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Dexamethasone (1 mg/kg s.c. at -18 h and -1 h) attenuated the effect endotoxin on the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in all tissues investigated, but did not significantly influence expression of lipocalin prostaglandin D synthase mRNA in spinal cord and dorsal root ganglia. | |||||||||||||||
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These higher levels of anti-inflammatory prostaglandin correlated with higher expression of its specific enzymatic source, lipocalin prostaglandin D synthase (PGDS) in the S and EAE+S groups (western blot analysis in figure 4C with densitometric analysis of the band, F: 19,88, dF: 7). | |||||||||||||||
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We quantitated mRNA levels for enzymes involved in the prostaglandin biosynthetic pathways and found that both COX-2 and PGE synthase (PGEs) mRNA levels were increased in the brain; no changes were found for expression of COX-1 or PGD synthase mRNA. | |||||||||||||||
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In the control rats, 4 kinds of PGs, i.e., 6-keto-PGF1 alpha, PGF2 alpha, PGE2 and PGD2, were detected in gastric mucosa, but no LT was detected. | |||||||||||||||
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Likewise, PGH2, a common precursor of PGs, appears to be selectively consumed by the PGE2 pathway rather than the PGI2 and PGD2 pathways, thereby producing PGE2 in the spinal cords of EAE mice [43]. | |||||||||||||||
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Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats. | |||||||||||||||
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Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats. | |||||||||||||||
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We observed significant changes in expression of several key enzymes (3-alpha-hydroxysteroid dehydrogenase, phospholipase a2, prostaglandin d2 synthase, and COX2) involved in eicosanoid biosynthesis (Table 4, Arachidonic acid cascade and mediators of inflammation). | |||||||||||||||
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Among seven PGs tested at 10(-6) M, only PGE2, PGE1, PGA2, and 16,16-dimethyl PGE2 significantly enhanced LH-RH secretion. 8-iso PGE2 weakly stimulated LH-RH secretion, whereas PGF2 alpha and PGD2 were ineffective. | |||||||||||||||
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In the COX pathway, enzymes convert PGH2 to the major physiologically active products, PGD2, PGE2, PGF2? | |||||||||||||||
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General Comments
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