Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Bergenin, a bioactive compound from Bergenia purpurascens, ameliorates psoriasis by targeting γδT17 cells via PPARγ-mediated PROX1 ubiquitination and degradation.
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Lin Haochang, Guo Yilei, Wan Xuanming, He Yue, Zhu Yanrong, Wei Zhifeng, Xia Yufeng, Dai Yue
Аннотация
BACKGROUND: Psoriasis, a persistent inflammatory skin ailment, is distinguished by aberrant γδT17 cell activation. The primary active compound in Bergenia purpurascens, bergenin (Ber), a natural peroxisome proliferator-activated receptor-gamma (PPARγ) agonist, appears to exhibit anti-γδT17 cell activation effects; nevertheless, its therapeutic efficacy for psoriasis remains to be elucidated.
PURPOSE: To investigate the effects of Ber on psoriasis and to explore its anti-psoriatic mechanisms of action.
METHODS: The effects of Ber activation of PPARγ on psoriasis and its γδT17 cells were assessed both in vitro and in vivo. The PPARγ and γδT17 cells activation in psoriatic patients and an imiquimod-induced C57BL/6 mouse model were evaluated. The fatty acid oxidation (FAO) was examined, and prospero homeobox protein 1 (PROX1) degradation and its impact on IL17A transcription were determined by Seahorse metabolic analysis, Co-IP, and ChIP-qPCR.
RESULTS: Ber alleviated psoriatic dermatitis by reducing γδT17 activation in a PPARγ-dependent manner, an effect abolished by adoptive transfer of activated γδT17 cells. Mechanistically, Ber-induced PPARγ activation enhanced its E3 ligase function, promoting K248-linked ubiquitination and degradation of PROX1. This inhibited CPT1-driven FAO, diminished histone H3K9/27 acetylation at the IL17A promoter, and repressed IL-17A production.
CONCLUSION: Ber exerts anti-psoriatic effects by activating PPARγ to prompt ubiquitin-mediated PROX1 degradation, thereby inhibiting FAO and IL-17A in γδT17 cells. This finding provides a novel pharmacological mechanism in support of the potential of Ber as a natural therapeutic agent.
PURPOSE: To investigate the effects of Ber on psoriasis and to explore its anti-psoriatic mechanisms of action.
METHODS: The effects of Ber activation of PPARγ on psoriasis and its γδT17 cells were assessed both in vitro and in vivo. The PPARγ and γδT17 cells activation in psoriatic patients and an imiquimod-induced C57BL/6 mouse model were evaluated. The fatty acid oxidation (FAO) was examined, and prospero homeobox protein 1 (PROX1) degradation and its impact on IL17A transcription were determined by Seahorse metabolic analysis, Co-IP, and ChIP-qPCR.
RESULTS: Ber alleviated psoriatic dermatitis by reducing γδT17 activation in a PPARγ-dependent manner, an effect abolished by adoptive transfer of activated γδT17 cells. Mechanistically, Ber-induced PPARγ activation enhanced its E3 ligase function, promoting K248-linked ubiquitination and degradation of PROX1. This inhibited CPT1-driven FAO, diminished histone H3K9/27 acetylation at the IL17A promoter, and repressed IL-17A production.
CONCLUSION: Ber exerts anti-psoriatic effects by activating PPARγ to prompt ubiquitin-mediated PROX1 degradation, thereby inhibiting FAO and IL-17A in γδT17 cells. This finding provides a novel pharmacological mechanism in support of the potential of Ber as a natural therapeutic agent.