INT55342
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Both Vimang and mangiferin showed inhibitory effects on macrophage activity: (a) intraperitoneal doses of only 50-250 mg/kg markedly reduced the number of macrophages in peritoneal exudate following intraperitoneal injection of thioglycollate 5 days previously (though there was no significant effect on the proportion of macrophages in the peritoneal-exudate cell population); (b) in vitro concentrations of 0.1-100 microg/ml reduced the phagocytosis of yeasts cells by resident peritoneal and thioglycollate-elicited macrophages; (c) in vitro concentrations of 1-50 microg/ml reduced nitric oxide (NO) production by thioglycollate-elicited macrophages stimulated in vitro with lipopolysaccharide (LPS) and IFNgamma; and (d) in vitro concentrations of 1-50 microg/ml reduced the extracellular production of reactive oxygen species (ROS) by resident and thioglycollate-elicited macrophages stimulated in vitro with phorbol myristate acetate (PMA). | |||||||||||||||
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It is concluded that capsaicin or curcumin in combination with dietary fatty acids differentially lowers the production of ROS in macrophages. | |||||||||||||||
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Capsaicin and curcumin feeding further lowered the generation and release of ROS. | |||||||||||||||
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With propofol infusion, there was decreased ROS production from the reperfused liver, with less hepato-cellular injury, followed by well-maintained pulmonary function. | |||||||||||||||
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This study shows good agreement between different methods of determining ROS formation, and that inhibition of ROS formation in vivo is paralleled by a decrease in inflammation. | |||||||||||||||
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Antioxidants significantly inhibited ROS generation. | |||||||||||||||
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Except for naproxen, NSAIDs reduced ROS production: 58 +/- 2% diclofenac, 90 +/- 2% indomethacin, 33 +/- 3% piroxicam, and 45 +/- 6% tenoxicam (N = 6). | |||||||||||||||
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This cardioprotective activity of ALA might be associated with an anti-apoptotic effect of ALA via suppression of ROS generation, increase of pERK 1/2 and decrease of pJNK 1/2 activity.
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However, ROS are formed in excessive amounts within the first few minutes following reperfusion and are considered a major factor involved in myocardial reperfusion injury.5)21-23) To minimize reperfusion injury, powerful antioxidants have been administered to reduce ROS generation and thereby decrease myocardial injury.17)24)25) Among the antioxidants, ALA, a thiol compound, is a cofactor for mitochondrial dehydration enzymes. | |||||||||||||||
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These findings suggest that the cardioprotective effects of ALA might be closely associated with the suppression of apoptosis due to decreased generation of ROS. | |||||||||||||||
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On polarized light microscopy, using a detector for active oxygen, CM-H2DCFDA, in the ALA 25 mg/kg group compared to the control group, showed that the generation of ROS was significantly suppressed at the site of myocardial infarction (p<0.0001). | |||||||||||||||
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As such, a more effective approach is to enhance mitochondrial metabolism by reducing electron leakage with attendant reduction of ROS generation. | |||||||||||||||
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Determination of ROS formation | |||||||||||||||
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The highest ROS production was measured after 12 h treatment. | |||||||||||||||
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The increases in both [Ca(2+)](c) and ROS production were completely abolished in calcium-free buffer or by a TRPV1 antagonist capsazepine. | |||||||||||||||
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PZ prevented ROS production and the increase in protein S-oxidation. | |||||||||||||||
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Taken together these results suggests that acetaminophen may attenuate the age-associated increases in the cardiomyocyte apoptosis, possibly via diminishing age associated elevation in ROS production. | |||||||||||||||
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To summarise, it seems that AAP concentrations up to 100 µM or AAP doses up to 100 mg/Kg prevent ROS production and citotoxicity, but higher doses do not. | |||||||||||||||
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Interestingly, recent experiments in arthritis-prone rats found that animals with an altered form of one of the subunits of this complex, Ncf1, that decreased the production of ROS also had greater susceptibility to arthritis. | |||||||||||||||
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For example, it is not known whether reduced capacity to produce ROS is a significant factor in human RA. | |||||||||||||||
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General Comments
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