INT26736
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Overall, our results from the Fos-LI and behavior tests suggest that LO products released from inflamed tissues contribute to nociception during carrageenan-induced inflammation, indicating that the LO pathway is a possible target for modulating inflammatory pain. | |||||||||||||||
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Blockade by lipoxygenase inhibitors of Ca2+-dependent insulin secretion from permeabilized rat islets. | |||||||||||||||
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The decreased relaxation by BK in anococcygeus muscle did not occur by the release of cyclooxygenase products or tachykinins from tracheal epithelium, but it may have occurred by the contractile action of lipoxygenase product secreted by nonepithelial sources. | |||||||||||||||
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Co-localization of 5-LOX expression in neurons and microglia/macrophage in brain after IR injury.As inferred from the data above (Fig. 1E, ac), there is an increase in the expression of 5-LOX enzyme after IR injury. | |||||||||||||||
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The critical aspect of 5-LOX/NF-? | |||||||||||||||
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A co-localization study of 5-LOX and GFAP, a marker for activated astrocytes, showed a few 5-LOX/GFAP positive cells (Fig. 2f). | |||||||||||||||
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To determine the cellular localization of 5-LOX expression, sections from ischemic brain after 24 h of reperfusion were subjected to immunohistochemistry with antibody against 5-LOX. 5-LOX expression co-localized with NSE, a neuron specific marker, implying that 5-LOX protein expression was increased in neurons after IR (Fig. 2c). | |||||||||||||||
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In 3-oxo-TA-challenged PMNs, the mitogen-activated protein kinase kinase (MEK)-1/2 inhibitor PD098059 abolished 5-LO product formation, along with inhibition of MEK-1/2 phosphorylation and 5-LO translocation. | |||||||||||||||
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In our attempt to characterize the stimulating constituents, we identified the tetracyclic triterpene 3-oxo-tirucallic acid (3-oxo-TA), which, in the range from 2.5 to 15 microM, enhanced 5-LO product formation in ionophore-challenged polymorphonuclear cells (PMNs) (e.g., from 1981 +/- 177 to 3042 +/- 208 pmol at 10 microM 3-oxo-TA), and initiated Ca(2+) mobilization, MEK-1/2 phosphorylation, 5-LO translocation, and 5-LO product formation in resting cells (534 +/- 394 pmol/5 x 10(6) PMNs). | |||||||||||||||
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The acidic NSAID mofebutazone and its metabolite butyl malonic acid mono (1-phenylhydrazide) had no effect on the cardiac release of arachidonic acid-derived cyclo-oxygenase and lipoxygenase products. | |||||||||||||||
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General Comments
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