Effect of minocycline on acne inflammation via PPARγ/STAT3 pathway
YANG Xuefan
YE Feng
RUAN Dandan
MO Xiaohui
JU Qiang
Abstract：Objective To investigate the mechanism of minocycline in acne Inflammation by regulating peroxisome proliferator-activated receptor γ(PPARγ)/STAT3 signaling pathway.Methods An acne-like model was established by intradermal injection of Cutibacterium acnes into mice,followed by oral administration of mino-cycline or sterile water.Skin lesions were observed,and hematoxylin-eosin staining,immunohistochemistry,and immunofluorescence were performed to assess inflammatory cell infiltration and pathway-related factor expression.In parallel,SZ95 human sebocytes were stimulated with peptidoglycan(PGN)and treated with minocycline,with or without the PPARγ antagonist T0070907.Inflammatory cytokines(IL-1α,IL-1β,IL-6,IL-8)were quantified,and PPAR γ and STAT3 expression were analyzed.Results Minocycline treatment significantly alleviated skin inflammation in mice,reduced inflammatory cell infiltration,enhanced PPARγ expression,decreased IL-1β and MPO-positive cells,and significantly attenuated p-STAT3 immunoreactivity(P<0.05).In SZ95 sebocytes,PGN induced robust cytokine production and STAT3 phosphorylation.Minocycline treatment significantly suppressed pro-inflammatory cytokines,upregulated PPARγ,and inhibited STAT3 activation,whereas the presence of T0070907 partially reversed these effects.Conclusions Minocycline exerts anti-inflammatory effects in acne by activating the PPARγ/STAT3 pathway,thereby dampening cytokine release and neutrophil infiltration.These findings high-light PPARγ as a potential therapeutic target and provide mechanistic insight into the anti-inflammatory benefits of minocycline in acne management.
Keywords：acne vulgarisminocyclinePPARγinflammatory cytokinessebocytes
Publication Date：2026-01-25
Online Publishing Date：2026-01-28(First online date of this platform, not the publication date of the document)
Pages：8( 212-219 )