Antibacterial. Specific inhibitor of CYP2C9. Blocks pro-inflammatory and atherogenic effects of linoleic acid (increase in oxidative stress and activation of AP-1) mediated by CYP2C9. Specific inhibitor of CYP2C9. Blocks pro-inflammatory and atherogenic effects of linoleic acid (increase in oxidative stress and activation of AP-1) mediated by CYP2C9. Inhibits bradykinin-induced tPA release.
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Bottomless glass bottle. Contents are inside inserted fused cone.
The Journal of physiology, 590(15), 3523-3534 (2012-06-08)
While it is accepted that NO is responsible for ∼60% of the plateau in cutaneous thermal hyperaemia, a large portion of the response remains unknown. We sought to determine whether the remaining ∼40% could be attributed to EDHF-mediated activation of
The objective of this study was to establish the cardioprotective effect of sulfaphenazole (SPZ), a selective inhibitor of cytochrome P450 2C9 enzyme, in an in vivo rat model of acute myocardial infarction (MI). MI was induced by 30 min ligation
The Journal of clinical endocrinology and metabolism, 95(2), 920-927 (2009-12-22)
The aim of this study was to assess whether patients with primary hyperparathyroidism (PHPT) show reduced endothelial function and to determine the mechanisms involved. The impact of parathyroidectomy (PTx) on endothelial function was also assessed. Endothelial dysfunction is reported in
Journal of pharmaceutical and biomedical analysis, 97, 65-71 (2014-05-13)
This is a report about the investigation of the metabolic fate of m-nisoldipine in human liver microsomes and the recombinant cytochrome P450 enzymes by using LC-MS/MS. A sensitive and reliable LC-MS/MS method was developed to obtain a rapid and complete
American journal of physiology. Heart and circulatory physiology, 298(2), H570-H579 (2009-12-17)
Previously, we showed that sulfaphenazole (SUL), an antimicrobial agent that is a potent inhibitor of cytochrome P4502C9, is protective against ischemia-reperfusion (I/R) injury (Ref. 15). The mechanism, however, underlying this cardioprotection, is largely unknown. With evidence that activation of autophagy
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