FLUNISOLIDE

Flunisolide hemihydrate is a corticosteroid, which is an orally active glucocorticoid receptor activator with anti-inflammatory activity. Flunisolide hemihydrate can induce eosinophil apoptosis, and is used for the research of asthma or rhinitis, and inflammation[1][2].

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Endocrinology

Research Areas >> Inflammation/Immunology

Signaling Pathways >> GPCR/G Protein >> Glucocorticoid Receptor

Flunisolide hemihydrate (0.1-10 μM, 1 h) inhibits lung fibroblast (Isolated from lung) activation[1]. Flunisolide hemihydrate (10 μM, 24 h) reduces MMP-9, TIMP-1, TGF-β and fibronectin release by sputum cells (isolated frommild to moderate asthmatics), and induces sputum eosinophil apoptosis[2]. Flunisolide hemihydrate (0.1-10 µM μM, 24 h) effectively inhibits ICAM-1 expression and GM-CSF and IL-5 release induced by TNF-alpha in BEAS-2B cells[3]. Flunisolide hemihydrate (115 µM, 0-3 h) can be transported in a polarized way in the apical (ap) to basolateral (bl) direction in Calu-3 cells and is demonstrated to be ATP-dependent[4]. Apoptosis Analysis[2] Cell Line: Eosinophil Concentration: 10 μM Incubation Time: 24 h Result: Induced sputum eosinophil apoptosis.

Flunisolide hemihydrate (Intranasal administration, 0.3-10 µg/mouse, daily, from days 21–27) inhibits lung inflammation, fibrosis, and airway hyper-reactivity, also improves clearance of silica particles from the lungs in silicotic mice[1]. Flunisolide hemihydrate (Intranasal administration, 0.3-10 µg/mouse, daily, from days 21–27) inhibits silica-induced macrophage and myofibroblast accumulation in the lung tissue[1]. Animal Model: Male Swiss Webster mice (instilled, intranasally, with crystalline silica, 10 mg/50 µL, particle size 0.5-10 µm)[1] Dosage: 0.3-10 µg/mouse, daily, from days 21–27 Administration: Intranasal administration Result: Reduced both granulomatous response, collagen deposition, concerning granuloma formation caused by silica particles. Reduced the number of F4/80 and α-SMA positive cells.

[1]. Tatiana Paula Teixeira Ferreira, et al. Intranasal Flunisolide Suppresses Pathological Alterations Caused by Silica Particles in the Lungs of Mice. Front Endocrinol (Lausanne). 2020 Jun 17;11:388.

[2]. M Profita, et al. In vitro effects of flunisolide on MMP-9, TIMP-1, fibronectin, TGF-beta1 release and apoptosis in sputum cells freshly isolated from mild to moderate asthmatics. Allergy. 2004 Sep;59(9):927-32.

[3]. S Boero, et al. Modulation by flunisolide of tumor necrosis factor-alpha-induced stimulation of airway epithelial cell activities related to eosinophil inflammation. J Asthma. 2010 May;47(4):381-7.

[4]. B I Florea, et al. Evidence of P-glycoprotein mediated apical to basolateral transport of flunisolide in human broncho-tracheal epithelial cells (Calu-3). Br J Pharmacol. 2001 Dec;134(7):1555-63.