| The influence of Moxifloxacin on the expression of iNOS and production of NO in vascular endothelial cellsObjectives:This study was designated to study the effect of Moxifloxacin on LPS-induced expression of Inducible Nitric Oxide Synthase (iNOS) and production of Nitric Oxide (NO), and to investigate the potential mechanism associated with nuclear factorκB (NF-κB) inhibition.Methods:Vascular endothelial cells EA.Hy926 were cultured in vitro and preincubated with 5-20 mg/L MXF before 0.1mg/L LPS stimulation to assay the production of NO with Griess reagents. The expressions of iNOS mRNA and protein were detected by RT-PCR and Western blot respectively. The inhibition of NF-κB induced by MXF in EA.Hy926 cells was assessed by Western blot, the effects of pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, on the production of NO and the expressions of iNOS protein were also examined.Results:MXF inhibits LPS-induced expressions of iNOS mRNA and protein and thus produces NO in dose-dependent manner in vascular endothelial cells. In the 5mg/L of MXF group, LPS stimulated EA.Hy926 cells induction of NO (26.3±3μM); when the MXF concentration reached 20mg/L, the NO decreased to (18.1±1.4)μM, with the inhibition rate of 42%. The protein of iNOS and the levels of NO were inhibited in response to LPS associated with PDTC, an inhibitor of NF-κB. The activation of NF-κB was inhibited in EA.Hy926 cells after 2 h treated with MXF, which led to the decreased p65 level in the nucleus.Conclusion:1. MXF could inhibit LPS-induced expression of iNOS and production of NO in EA.Hy926 cells. 2. MXF could inhibit NF-κB activation in EA.Hy926 cells.3. MXF inhibit LPS-induced expression of iNOS and production of NO, potentially resulting from inhibition of NF-κB. |