INT293
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The degradation of two peptides, Leu-enkephalin (Enk) and Tyr-Pro-Leu-Gly amide (TPLG), during skin penetration and on the dermal side following penetration, and the prevention of degradation by some protease inhibitors, were investigated using rat skin in vitro. | |||||||||||||||
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The degradation of two peptides, Leu-enkephalin (Enk) and Tyr-Pro-Leu-Gly amide (TPLG), during skin penetration and on the dermal side following penetration, and the prevention of degradation by some protease inhibitors, were investigated using rat skin in vitro. | |||||||||||||||
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In fact, enzymes involved in enkephalin degradation were decreased during perfusion (39%) and increased during ischemia (50%). | |||||||||||||||
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The effect of ischemia on cardiac Leucine enkephalin (Leu-enk) content, degradation and coronary release was studied in the isolated perfused hearts of male Sprague Dawley rats. | |||||||||||||||
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The influence of the catecholamine hormones and some of their metabolites on the enzymatic degradation of met-enkephalin by rat brain homogenates has been evaluated. | |||||||||||||||
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Inhibition of the enzymatic degradation of Met-enkephalin by catecholamines. | |||||||||||||||
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Boroleucine prolonged the leucine enkephalin degradation half-life 1.6-1.9-fold in each medium at 0.1 microM concentrations, 1/1000th the concentration of leucine enkephalin. | |||||||||||||||
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These observations suggest that inhibitors of enkephalinase A produce analgesia through a pharmacological mechanism which is not directly related to inhibition of enkephalin degradation. | |||||||||||||||
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Since the major pathway of enkephalin degradation seems to occur under the action of aminopeptidases, in the present paper we describe the changes in Tyr-aminopeptidase activities during several stages of the rat (male and female) brain development (9, 12, 15, 20 and 25 days postbirth). | |||||||||||||||
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Characterization of enkephalin degradation in rat plasma. | |||||||||||||||
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Differential posttranslational processing of proenkephalin in rat bone marrow and spleen mononuclear cells: evidence for synenkephalin cleavage. | |||||||||||||||
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Enkephalin degradation includes an enkephalinase (EC 3.4.24. 11) and the effects on the colic electromyographic profile of its inhibition by acetorphan has been investigated in the unrestrained rat. | |||||||||||||||
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In addition, the chelator 1,10-phenanthroline was also capable of effectively inhibiting enkephalin degradation, suggesting that the enzyme responsible has the characteristics of a metalloprotease. | |||||||||||||||
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This was confirmed by the ability of bestatin, a specific inhibitor of cell surface aminopeptidases, to almost completely inhibit enkephalin degradation by splenocytes (85%) and A-NK cells (96%). | |||||||||||||||
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The degradation of the enkephalin-containing octapeptide Tyr-Gly-Gly-Phe-Met-Arg-Gly-Leu (YGGFMRGL) was systematically investigated by incubating the peptide with synaptic membranes from rat striatum or with purified peptidases. | |||||||||||||||
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It was assumed that enkephalinase B functions mainly in enkephalin degradation in vivo. | |||||||||||||||
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On a cellular basis, enkephalin degradation was four to five times greater with A-NK cells than with splenocytes. | |||||||||||||||
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These results suggest that potentiation of analgesia by bestatin may be due to the protection against the degradation of kyotorphin and released enkephalin by a membrane-bound aminopeptidase. | |||||||||||||||
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The results show that the analgesic effect of anticholinesterases are more likely due to mechanisms other than inhibition of enkephalin degradation. | |||||||||||||||
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Based on the assumption that non-opioid systems may mask the activity of opioid analgesia systems, we attempted to either enhance opioid analgesia by: preventing enkephalin degradation by the use of D-phenylalanine; increasing the entry of blood-borne opioids into the brain by the use of DMSO; and the attenuation of non-opioid analgesia by the use of reserpine. | |||||||||||||||
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General Comments
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