Meconopsis quintuplinervia Regel Improves Cutibacterium acnes-Induced Inflammatory Responses in a Mouse Ear Edema Model and Suppresses Pro-Inflammatory Chemokine Production via the MAPK and NF-κB Pathways in RAW264.7 Cells.

Abstract

Acne vulgaris (AV) is a common adolescent skin condition which is mainly caused by Cutibacterium acnes overcolonization and subsequent inflammation. Our previous studies demonstrated that ethanol extracts of Meconopsis quintuplinervia Regel (EMQ) possess significant antimicrobial properties. However, their protective effects and potential mechanisms against AV remain unclear. In the present study, the EMQ treatment potential for AV was evaluated in a C. acnes-induced mouse ear edema model, and the EMQ anti-inflammatory mechanism was evaluated in lipopolysaccharide (LPS)-induced RAW264.7 macrophage cells. The results showed that EMQ alleviated edema formation and inflammatory cell infiltration in an acne mouse model by suppressing inflammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor α expression. Moreover, EMQ inhibited the phosphorylation of MAP kinases (MAPKs) such as p38, JNK, and ERK, the phosphorylation and degradation of IκB-α and the nuclear translocation of nuclear factor kappa B (NF-κB) p65 in LPS-induced RAW264.7 cells. These findings suggest the potent anti-inflammatory activity of EMQ is possibly through the regulation of the MAPKs and NF-κB signaling pathways. Inhibition of C. acnes activity combined with a powerful anti-inflammatory effect of EMQ indicated its potential as a novel therapeutic option for AV.