Evidence for sodium azide as an artifact mediating the modulation of inducible nitric oxide synthase by C-reactive protein.

摘要: C-reactive protein (CRP) is an acute-phase identified as a cardiovascular risk marker. In recent years, increasing number of studies have investigated the possible direct effects CRP on vasculature, using mainly commercial CRP. present work, potential role for modulator inducible nitric oxide synthase (iNOS) induction was explored. Cultured human aortic vascular smooth muscle cells (HASMC) were stimulated 18 hours with 10 ng/mL interleukin-1beta (IL-1beta), resulting in marked increase iNOS levels and NO production, determined by Western blotting nitrite measurement, respectively. Commercial (1 to 100 microg/mL) concentration-dependently inhibited elicited IL-1beta. Unexpectedly, similar results observed when solution replaced corresponding vehicle medium containing growing concentrations sodium azide. The inhibitory or lost azide removal dialysis. conclusion, from solution, but not itself, accounts effect IL-1beta-evoked release. Care should be taken before attributing any biologic