Glucocorticoids are considered the main treatment option for @entity480 , but their effect is only recently being understood. AIM: To evaluate whether @entity5023 (FP) inhibits the inflammatory process induced by @entity310 in vitro, and to assess if @entity2451 is associated to this inhibition. STUDY DESIGN: Experimental in vitro study. MATERIALS AND METHODS: Nasal polyp fibroblasts were cultured during 24 hours. Three different concentrations of FP (1, 10 and 100 nM, added to @entity310 ) were compared to negative (without additive) and positive ( @entity310 ) controls. Gene expression (RTQ-PCR) and protein concentration (ELISA) of @entity4725 , @entity2071 , eotaxin and @entity5737 were measured, as well as the nuclear translocation of @entity2451 . RESULTS: @entity310 significantly increased protein concentration and RNA expression of all the studied molecules, as well as the nuclear translocation of @entity2451 , when compared to the negative control. FP decreased these parameters in a dose-dependent manner, statistically different from positive control up to 100nM. CONCLUSIONS: FP extensively inhibited inflammatory recruiters, at both protein and RNA levels, confirming the ability of glucocorticoids to modulate the inflammatory process in @entity480 . This inhibition was associated to decreased @entity2451 nuclear translocation, demonstrating that this is an important mechanism of glucocorticoids action for @entity480 .

In vitro effect of glucocorticoids on XXXX .

@entity5737 :: ('6352', 'Gene') :: ['RANTES'] @entity2451 :: ('4790', 'Gene') :: ['NF-kappaB'] @entity310 :: ('7124', 'Gene') :: ['TNF-alpha'] @entity4725 :: ('7412', 'Gene') :: ['VCAM-1'] @entity480 :: ('MESH:D009298', 'Disease') :: ['nasal polyps'] @entity2071 :: ('3383', 'Gene') :: ['ICAM-1'] @entity5023 :: ('MESH:C065382', 'Chemical') :: ['fluticasone propionate']
@entity480 :: (MESH:D009298,Disease) :: ['nasal polyps']
