Rebamipide suppresses TNF-α mediated inflammation in vitro and attenuates the severity of dermatitis in mice

Abstract

Rebamipide is a routine drug for the treatment of gastritis in a clinical setting. Recently, it has been shown to protect against various inflammatory diseases, and has provided a potential therapy for these diseases. However, whether rebamipide has a role in dermatitis remains to be elucidated. Here, we found that rebamipide alleviated the inflammatory reaction induced by tumor necrosis factor-α in RAW264.7, a stable macrophage cell line. Furthermore, rebamipide treatment repressed activation of nuclear factor-kappaB signaling, a well-established inflammatory signaling pathway. Moreover, an oxazolone-induced dermatitis mouse model was established to investigate the role of rebamipide in vivo. PBS control group exhibited typical skin inflammation, whereas treatment with rebamipide remarkably attenuated a dermatitis phenotype in this mouse model. The protective role of rebamipide in dermatitis in vivo was probably due to its inhibition of nuclear factor-kappaB signaling. Collectively, rebamipide may represent a promising molecular target for the prevention and treatment of inflammatory skin diseases. Rebamipide is a routine drug for gastritis in clinic, but it is unknown whether it affects skin inflammation. Here, we found that rebamipide alleviated TNF-α mediated inflammatory reaction induced in macrophage. Rebamipide repressed activation of NF-κB signaling. Moreover, rebamipide attenuated dermatitis phenotype in oxazolone induced dermatitis mice model. Collectively, rebamipide may represent a promising molecular target for inflammatory skin diseases.