Mahdi Alsugoor
Umm Al Qura University, Saudi Arabia
Title: Fluticasone propionate attenuate induced nitric oxide synthase through dephosphorylation of p38 and Akt
Biography
Biography: Mahdi Alsugoor
Abstract
The upregulation of the inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production have been implicated in inflammatory pathologies. Although research has revealed that non selective glucocorticoids (GCs) such as dexamethasone and hydrocortisone inhibit iNOS expression and NO production, the selective GCs , fluticasone propionate, action on iNOS expression and function remain to be investigated. In addition, investigations were performed to distinguish the GC and non-GC actions using receptor antagonists. Since the effects of GCs on upstream signalling pathways remain vague, further studies were conducted to investigate whether fluticasone regulates the p38 mitogen-activated protein kinases or protein kinase B (Akt) pathways, both of which have been reported to be critical for the induction of iNOS.
Methodology: All experiments were conducted using primary cultures of rat aortic smooth muscle cells (RASMCs). The cells were activated with bacterial LPS (100 μg/mL) and interferon-gamma (IFN-γ, 100 U/mL) to induce iNOS and NO. Nitrite levels in cellular supernatants were quantified by the Griess assay, and expressions of iNOS , phospho-p38 (P-p38) and phospho-Akt (P-Akt) were investigated by western blotting.