INT96365
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
GCs were abolished by electrical field stimulation, S-nitroso-N-acetyl-penicillamine, and 8-bromo-cGMP. | |||||||||||||||
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Constitutive release of nitric oxide from enteric neurons sustains cGMP synthesis in the colonic smooth muscle to suppress spontaneous in vitro GCs. | |||||||||||||||
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The GCs were unaffected by hexamethonium, atropine, and antagonists of serotonergic (5-HT(1--4)), histaminergic (H(1--2)), and tachykininergic (NK(1--2)) receptors but enhanced by NK(3) receptor antagonism. | |||||||||||||||
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However, NAC is only protective as long as a viable cysteine-driven synthesis of GSH is operative [25] since it is ineffective when the hepatic store of GSH is artificially depleted by a treatment with buthionine sulfoximine, an inhibitor of GCS [18,39]. | |||||||||||||||
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Protection by NAC, HYTAU and TAU against APAP-induced liver injury is also a reflection of their ability to prevent the loss of GCS activity to a toxic dose of APAP, an enzyme that plays a crucial role in protecting the liver against hepatotoxic compounds by regulating the de novo synthesis of GSH. | |||||||||||||||
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The results summarized in Figure 5, 6, 7 indicate that a toxic dose of APAP lowered the plasma activities of GR, GST and GCS, respectively, and that all the test compounds offered different degrees of protection against such losses. | |||||||||||||||
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-GCS knockdown rats [56] or a specific inhibitor of GCS activity such as buthionine sulfoximine [18] and in which hepatotoxicity by APAP was more extensive than in normal or uninhibited animals. | |||||||||||||||
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Although there are previous reports about the inhibitory effect of GCs on IFN-? | |||||||||||||||
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General Comments
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