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Quercetin confers protection against psoriasis by inhibiting AKR1B10-mediated glycolytic reprogramming in
Huiqin Wang1, Yanwen Liu2, Yuan Ding1
1Department of Dermatology and Venereology, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Clinical Research Center for Dermatology and Venereology, Xinjiang Key Laboratory of Dermatology Research, Urumqi, 830000, China.
Abstract:
The anti-psoriatic effect of quercetin has been observed. However, the involved mechanism remains poorly explored. Hence, the study investigated the therapeutic effects of quercetin against psoriasis and elucidated its underlying molecular mechanisms, with a focus on AKR1B10-mediated glycolytic reprogramming. An imiquimod (IMQ)-induced mouse model and an interleukin-17A (IL-17A)-stimulated keratinocyte model were established as psoriasis-like models. Therapeutic effects of quercetin on psoriasis-like lesions were evaluated by gross lesion observation, PASI scoring, histopathological staining, and immunohistochemistry. Flow cytometry as well as ELISA were performed to assess T helper 17 (Th17) cell proportions and systemic inflammatory responses. Candidate therapeutic targets of quercetin in psoriasis treatment were obtained by integrating GEO database analysis, target prediction, and machine learning algorithms. A series of assays were harnessed to measure AKR1B10 expression and glycolysis-related enzymes, lactic acid, and extracellular acidification rate (ECAR). AKR1B10 overexpression experiments were performed to validate the function of AKR1B10. Quercetin markedly alleviated psoriasis-like skin lesions and repressed inflammation in IMQ-treated mice, accompanied by significantly inhibited Th17 cell expansion and keratinocyte hyperproliferation and reduced levels of inflammatory cytokines. AKR1B10 was identified as a potential mediator of quercetin activity in psoriasis, which was upregulated in psoriasis. Mechanistically, quercetin lowered AKR1B10 expression, downregulating key glycolytic enzymes and lactic acid and reducing ECAR. Overexpressing AKR1B10 largely negated suppressive impacts of quercetin on keratinocyte glycolysis and proliferation. Quercetin alleviates inflammation and abnormal keratinocyte proliferation in experimental psoriasis-like models, potentially through modulation of AKR1B10-associated glycolytic reprogramming.