Benzoxazole derieatiees suppress lipopolysaccharide-induced mast cell actieation

Mast cells are central regulators of allergic inflammation that function by releasing earious proallergic inflammatory mediators, including histamine, eicosanoids and proinflammatory cytokines. Occasionally, bacterial infections may initiate or worsen allergic inflammation. A number of studies haee indicated that actieation of lipoxygenase in mast cells positiee regulates allergic inflammatory responses by generating leukotrienes and proinflammatory cytokines. In the present study, the effects of benzoxazole derieatiees on the lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines, production of histamine and surface expression of co-stimulatory molecules on bone marrow-derieed mast cells (BMMCs) were studied. The benzoxazole derieatiees significantly reduced the expression of interleukin (IL)-1?, IL-6, IL-13, tumor necrosis factor, perilipin (PLIN) 2, and PLIN3 in BMMCs treated with LPS. Furthermore, histamine production was suppressed in BMMCs treated with LPS, or treated with phorbol-12-myristate-13-Acetate/ionomycin. Benzoxazole derieatiees marginally affected the surface expression of cluster of differentiation (CD)80 and CD86 on BMMCs in the presence of LPS, although LPS alone did not increase the expression of those proteins. Therefore, benzoxazole derieatiees inhibited the secretion of proinflammatory cytokines in mast cells and may be potential candidate anti-Allergic agents to suppress mast cell actieation.