Benvitimod Ameliorates Rosacea-Like Eruptions in Mice and Suppresses the TLR Pathway in Keratinocytes
Traditional treatments for rosacea are quite limited with high recurrence rates. A more reliable and targeted therapy is urgently needed. We conducted this study to evaluate the underlying mechanisms of benvitimod on rosacea in vivo and invito. Benvitimod ameliorated LL37-induced rosacea-like eruptions in mice as indicated by reductions in redness scores and areas as well as in dermal inflammatory cell infiltrates. Elevated expressions of CXCL9, CXCL10 and CXCL11 following LL-37 treatment in these mice were decreased by benvitimod. In HaCaT cells receiving LL-37, TLR2 and chemokines were up-regulated, and levels of chemokines were further enhanced in LL-37 induced HaCaT cells overexpressing TLR2. In response to a regiment of 10 μM benvitimod for 8h, gene expressions of TLR2 and the CXCL9, CXCL10 and CXCL11 chemokines were decreased. In addition, protein expressions of these indices were decreased in response to 10 μM benvitimod for 24h. Benvitimod is beneficial in the treatment of LL-37-induced rosacea as demonstrated in mice and HaCaT cells. These findings not only suggest that benvitimod may provide a potential new therapeutic agent for the treatment of rosacea, but also indicate some of the mechanisms involved with these beneficial effects.