Journal of ethnopharmacology · 2026
Jinhuang San alleviates plasma cell mastitis by restoring Th17/Treg balance through the HTR7/IL-6/JAK2/STAT3 axis.
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Meng Ziqi, Liu Mengli, Weng Xiyu, Wu Linfeng, Wu Huanglei, Xue Rong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Jinhuang San (JHS) is a traditional topical medication for "mastitis". It is currently used in the treatment of plasma cell mastitis (PCM), but its mechanism remains unclear.
AIM OF THE STUDY: This study aimed to investigate the therapeutic mechanism of JHS in PCM through chemical characterization, immune microenvironment analysis, and experimental validation.
MATERIALS AND METHODS: The chemical constituents of JHS were characterized by UPLC-Q-Orbitrap-MS/MS. A PCM-like mouse model was established by intraductal injection of human PCM-derived breast tissue homogenate emulsified with complete Freund's adjuvant. JHS was topically administered for 7 consecutive days. Transcriptomic sequencing and public single-cell RNA-seq data were integrated to profile the immune microenvironment. A macrophage-CD4+ T cell co-culture system was established, and LP-44 (a selective HTR7 agonist) together with recombinant IL-6 was used for mechanistic validation. An in silico HTR7 perturbation analysis was also performed.
RESULTS: 30 major constituents were identified in JHS. Single-cell reanalysis indicated prominent macrophage infiltration and Th17/Treg imbalance in PCM. Molecular docking suggested potential interactions between several identified constituents and HTR7. In vivo and in vitro experiments showed that JHS reduced HTR7 expression, decreased IL-6 production, and attenuated JAK2/STAT3 phosphorylation; these effects were partially reversed by LP-44 or recombinant IL-6. Virtual HTR7 knockout altered immune-related genes (IL-6, JAK2, STAT3, FOXP3) and enriched Th17 pathways.
CONCLUSION: JHS alleviated experimental PCM and restored Th17/Treg balance, potentially through modulation of the HTR7/IL-6/JAK2/STAT3 axis in macrophages. These findings provide an experimental basis for further clinical evaluation of JHS in PCM.
AIM OF THE STUDY: This study aimed to investigate the therapeutic mechanism of JHS in PCM through chemical characterization, immune microenvironment analysis, and experimental validation.
MATERIALS AND METHODS: The chemical constituents of JHS were characterized by UPLC-Q-Orbitrap-MS/MS. A PCM-like mouse model was established by intraductal injection of human PCM-derived breast tissue homogenate emulsified with complete Freund's adjuvant. JHS was topically administered for 7 consecutive days. Transcriptomic sequencing and public single-cell RNA-seq data were integrated to profile the immune microenvironment. A macrophage-CD4+ T cell co-culture system was established, and LP-44 (a selective HTR7 agonist) together with recombinant IL-6 was used for mechanistic validation. An in silico HTR7 perturbation analysis was also performed.
RESULTS: 30 major constituents were identified in JHS. Single-cell reanalysis indicated prominent macrophage infiltration and Th17/Treg imbalance in PCM. Molecular docking suggested potential interactions between several identified constituents and HTR7. In vivo and in vitro experiments showed that JHS reduced HTR7 expression, decreased IL-6 production, and attenuated JAK2/STAT3 phosphorylation; these effects were partially reversed by LP-44 or recombinant IL-6. Virtual HTR7 knockout altered immune-related genes (IL-6, JAK2, STAT3, FOXP3) and enriched Th17 pathways.
CONCLUSION: JHS alleviated experimental PCM and restored Th17/Treg balance, potentially through modulation of the HTR7/IL-6/JAK2/STAT3 axis in macrophages. These findings provide an experimental basis for further clinical evaluation of JHS in PCM.