Abstract

Rosacea is a chronic, relapsing inflammatory skin disease featured by abnormal activation of immune responses, vascular dysfunction and prominent permeability barrier alterations. Aspirin, as the first nonsteroidal anti-inflammatory drug (NSAID), is widely used for various inflammatory conditions due to its anti-inflammatory and anti-angiogenic properties. However, its effects on rosacea are unclear. In this study, we demonstrated that aspirin dramatically improved pathological phenotypes in LL37-induced rosacea-like mice. The RNA-sequencing analysis revealed that aspirin alleviated rosacea-like skin dermatitis mainly via modulating immune responses. Mechanically, we showed that aspirin decreased the production of chemokines and cytokines associated with rosacea, and suppressed the Th1- and Th17-polarized immune responses in LL37-induced rosacea-like mice. Besides, aspirin administration decreased the microvessels density and the VEGF expression in rosacea-like skin. We further demonstrated that aspirin inhibited the activation of NF-κB signaling and the release of its downstream pro-inflammatory cytokines. Collectively we showed that aspirin exerts a curative effect on rosacea by attenuating skin inflammation and angiogenesis, suggesting a promising therapeutic candidate for the treatment of rosacea.