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-κκB Pathways in RAW264.7 Cells
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Background: Acne vulgaris (AV) is a common adolescent skin condition which is mainly caused by Cutibacterium acnes overcolonization and subsequent inf lammation. Objective: Our previous studies demonstrated that ethanol extracts of Meconopsis quintu- plinervia Regel (EMQ) possess significant antimicrobial properties. However, their protec- tive effects and potential mechanisms against AV remain unclear. Methods: 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-inf lammatory mechanism was evaluated in lipopolysaccharide (LPS)-induced RAW264.7 macrophage cells. Results: The results showed that EMQ alleviated edema formation and inf lammatory cell infiltration in an acne mouse model by suppressing inf lammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor α expression. Moreover, EMQ inhibited the phos- phorylation 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. Conclusion: These findings suggest the potent anti-inf lammatory activity of EMQ is pos- sibly through the regulation of the MAPKs and NF-κB signaling pathways. Inhibition of C. acnes activity combined with a powerful anti-inf lammatory effect of EMQ indicated its potential as a novel therapeutic option for AV.
Abstract
Background: Acne vulgaris (AV) is a common adolescent skin condition which is mainly caused by Cutibacterium acnes overcolonization and subsequent inf lammation. Objective: Our previous studies demonstrated that ethanol extracts of Meconopsis quintu- plinervia Regel (EMQ) possess significant antimicrobial properties. However, their protec- tive effects and potential mechanisms against AV remain unclear. Methods: 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-inf lammatory mechanism was evaluated in lipopolysaccharide (LPS)-induced RAW264.7 macrophage cells. Results: The results showed that EMQ alleviated edema formation and inf lammatory cell infiltration in an acne mouse model by suppressing inf lammatory cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor α expression. Moreover, EMQ inhibited the phos- phorylation 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. Conclusion: These findings suggest the potent anti-inf lammatory activity of EMQ is pos- sibly through the regulation of the MAPKs and NF-κB signaling pathways. Inhibition of C. acnes activity combined with a powerful anti-inf lammatory effect of EMQ indicated its potential as a novel therapeutic option for AV.
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