Abstract

Atopic dermatitis is a relapsing inflammatory skin condition characterized by erythema, edema, excoriation, and skin dryness. Cilostazol, a quinolone derivative, exhibits strong non-classical immunomodulatory and anti-inflammatory actions. This research intended to investigate the attenuated role of cilostazol in a murine model of 2,4-Dinitrochlorobenzene (DNCB)-triggered atopic dermatitis. The experiment began by applying a single 1% DNCB dose topically to the dorsal skin of mice in all groups except the control group. A challenge phase began on day 4, with 0.5% DNCB applied three times per week for three weeks. The treatment began on day 10 and continued for 21 days. 50 male albino BALB/c mice were allocated to 5 groups: control (received no therapy), DNCB only, DNCB with vehicle-based cream, DNCB with tacrolimus (received 0.1% tacrolimus ointment), and DNCB with cilostazol (received 0.5% cilostazol cream). Topical cilostazol effectively attenuated DNCB-exacerbated atopic dermatitis-mimicking cutaneous lesions, as evidenced by decreased clinical dermatitis scores, upregulated immunohistochemical expression of skin barrier proteins like filaggrin in skin tissues, and improved histopathological alterations. Moreover, cilostazol significantly minimized serum IgE levels and skin tissue levels of proinflammatory cytokines such as interleukin (IL)-4 and IL-13. Cilostazol therapy also remarkably alleviated the production of oxidative malondialdehyde while boosting the antioxidative activity of reduced glutathione. In conclusion, cilostazol attenuates DNCB-driven atopic dermatitis-like dermatological lesions by targeting immunological, inflammatory, and oxidative biomarkers.

Key words: Atopic dermatitis, Cilostazol, DNCB, Mouse model, Eczema, Filaggrin