龙葵改善银屑病皮损的机制和活性成分
{"_":"Mechanisms and active components of in the amelioration of psoriatic lesions.","i":["Solanum nigrum"]}
{"_":"Mechanisms and active components of in the amelioration of psoriatic lesions.","i":["Solanum nigrum"]}
银屑病是一种常见的慢性炎症性皮肤病,模式识别受体尤其是NLRP3炎症小体在其发病机制中日益受到关注。龙葵(Solanum nigrum,SN)在传统及临床实践中被用于银屑病的治疗,但其治疗机制和关键活性成分尚不明确。本研究探讨了龙葵的抗银屑病作用机制并鉴定了其主要生物活性成分。利用公共转录组数据集和临床皮肤活检标本评估了银屑病中NLRP3炎症小体的活化情况。在咪喹莫特诱导的原发性和复发性银屑病样皮炎模型中评估了龙葵的治疗效果。对皮损皮肤进行批量RNA测序以鉴定龙葵调控的通路。通过UPLC-MS对龙葵进行化学表征,并通过分子对接和分子动力学模拟筛选候选活性化合物。在公共数据集和临床标本中,银屑病皮损中NLRP3炎症小体活化均持续升高。龙葵显著减轻了原发性和复发性模型中的疾病严重程度,减少了角质形成细胞过度增殖,并降低了全身炎症细胞因子水平。转录组分析显示,龙葵主要调控PRR/NLR相关信号通路。在机制上,龙葵抑制了NLRP3炎症小体活化并减少了IL-1β和IL-18的产生。综合化学、生物学和计算分析,鉴定出葫芦巴碱(trigonelline)是龙葵抗银屑病作用的主要活性成分。龙葵主要通过抑制NLRP3炎症小体信号通路改善银屑病样皮炎,其中葫芦巴碱被鉴定为关键贡献活性成分。这些发现为龙葵在银屑病中的治疗应用提供了机制支持。
Psoriasis is a prevalent chronic inflammatory skin disease in which pattern recognition receptors, particularly the NLRP3 inflammasome, are increasingly implicated in disease pathogenesis. Solanum nigrum (SN) has been used in traditional and clinical practice for psoriasis treatment, but its therapeutic mechanisms and key active constituents remain unclear. This study investigated the anti-psoriatic mechanisms of SN and identified its major bioactive component. NLRP3 inflammasome activation in psoriasis was evaluated using public transcriptomic datasets and clinical skin biopsies. The therapeutic effects of SN were assessed in imiquimod-induced primary and relapse psoriasis-like dermatitis models. Bulk RNA sequencing of lesional skin was performed to identify SN-regulated pathways. SN was chemically characterized by UPLC-MS, and candidate active compounds were prioritized by molecular docking and molecular dynamics simulation. NLRP3 inflammasome activation was consistently elevated in psoriatic lesions in both public datasets and clinical specimens. SN markedly alleviated disease severity in primary and relapse models, reduced keratinocyte hyperproliferation, and lowered systemic inflammatory cytokine levels. Transcriptomic analysis showed that SN mainly modulated PRR/NLR-related signaling pathways. Mechanistically, SN inhibited NLRP3 inflammasome activation and decreased IL-1β and IL-18 production. Integrated chemical, biological, and computational analyses identified trigonelline as a major active constituent contributing to the anti-psoriatic effects of SN. SN ameliorates psoriasis-like dermatitis primarily through suppression of NLRP3 inflammasome signaling, with trigonelline identified as a key contributory active component. These findings provide mechanistic support for the therapeutic application of SN in psoriasis.
Ya Chen, Tianyou Ma, Congcong Zhu, Zongguang Tai, Huijun Pan, Zhongjian Chen, et al. {"_":"Mechanisms and active components of in the amelioration of psoriatic lesions.","i":["Solanum nigrum"]}. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1801799.
Ya Chen, Tianyou Ma, Congcong Zhu, Zongguang Tai, Huijun Pan, Zhongjian Chen, et al (2026). {"_":"Mechanisms and active components of in the amelioration of psoriatic lesions.","i":["Solanum nigrum"]}. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1801799
Ya Chen, Tianyou Ma, Congcong Zhu, Zongguang Tai, Huijun Pan, Zhongjian Chen, et al. {"_":"Mechanisms and active components of in the amelioration of psoriatic lesions.","i":["Solanum nigrum"]}[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1801799.
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