INT22548
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Western blot analysis showed that AA significantly suppressed 150/145 kDa subunits of alpha-fodrin breakdown products (FBDP) in cortex, striatum, thalamus and hippocampus at 24 and 48 h post-HI, and also 120 kDa subunit of FBDP in all examined regions except for thalamus, which indicated that AA injection inhibited both calpain and caspase-3 activation. | |||||||||||||||
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Apoptosis was further confirmed by increased caspase 3 protein levels and positive terminal deoxyuridine nick end labeling histochemistry. | |||||||||||||||
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As compared to controls, DMI increased the resistance-to-extinction of CPP, attenuated immobility, and increased wall climbing behavior. | |||||||||||||||
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These results show that a morphine-induced CPP is persistent over time and can be reinstated by morphine after extinction. | |||||||||||||||
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Lidocaine reduced cytochrome c release and caspase-3 activation in the penumbra at 4 h and diminished DNA fragmentation in the penumbra at 24 h. | |||||||||||||||
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Apoptotic changes were evaluated by immunohistochemistry for cytochrome c release and caspase-3 activation and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) for DNA fragmentation. | |||||||||||||||
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Cytochrome c release and caspase-3 activation were detected at 4 and 24 h after ischemia and DNA fragmentation was detected at 24 h. | |||||||||||||||
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During the retention of morphine-induced CPP, a morphine-dose- and time-dependent elevation of DA and its metabolites was observed in the NAc. | |||||||||||||||
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However, in adapted mucosa after aspirin, activated caspase 3 and the number of apoptotic cells had returned to basal levels. | |||||||||||||||
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Secondly, there is a path where receptors form groups in a death-receptor path, forming death-inducing signaling complex and finally activating the Casp8 and Casp3 (caspase-3) genes [23]. | |||||||||||||||
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These findings suggest that morphine exposure during the first embryonic days may enhance the susceptibility of neuroblasts to apoptosis by upregulating the ratio of Bax to Bcl-2 protein expression and increasing downstream caspase-3 activity. | |||||||||||||||
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Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release. | |||||||||||||||
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In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated. | |||||||||||||||
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These results showed an increased ratio of Bax/Bcl-2 and activated caspase-3 in hippocampus and dorsal lumbar spinal cord of animals treated with pain and IMO stress; these effects were reduced in ADX animals. | |||||||||||||||
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High glucose also causes a 2 fold increase in Bax expression, which induced cytochrome C release which in turn stimulates apoptosis activating factor, caspase 9 and caspase 3 [41]. | |||||||||||||||
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Brain histopathology showed myelin disintegration and caspase-3 activation in glial cells, whereas, grey matter changes were sparse. | |||||||||||||||
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In a model of peripheral neuropathy, obtained by the loose ligation of the rat sciatic nerve (CCI), we describe a nerve apoptotic state that encompasses the release of cytochrome C in the cytosol, the activation of caspase 3, and the fragmentation of the genome. | |||||||||||||||
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Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. | |||||||||||||||
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Caspase-3 mRNA levels, estimated by semiquantitative RT-PCR, were elevated fivefold in ipsilateral cortex and twofold in hippocampus by 24 hr after TBI. | |||||||||||||||
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Reducing Na(+) entry with the VSSC blocker, tetrodotoxin (TTX), attenuated apoptotic neuronal death via a reduction in caspase-3 activation. | |||||||||||||||
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