Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels

Haiqing Long; Qiu Xiang; Zhuxuan Lan; Luxiang Bai; Shijin Yin

doi:doi:10.11648/j.sd.20251306.17

Research Article |

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Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels

Haiqing Long, Qiu Xiang, Zhuxuan Lan, Luxiang Bai, Shijin Yin^*

Published in Science Discovery (Volume 13, Issue 6)

Received: 5 November 2025 Accepted: 9 December 2025 Published: 24 December 2025

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Abstract

Objective: To investigate the blocking effect of licochalcone D on the voltage-gated potassium channel Kv1.3 and its potential therapeutic efficacy in psoriasiform skin inflammation, thereby providing experimental evidence for its use as an immunomodulatory candidate drug. Methods: The inhibitory effects of licochalcone D on exogenous and endogenous Kv1.3 currents were recorded by whole-cell patch-clamp. Ca²⁺ influx in Jurkat T cells was monitored with Fura-2 AM imaging. A ConA-induced T-cell activation model was established to quantify IL-2 secretion. An imiquimod-induced psoriasis-like mouse model was then established for in-vivo pharmacodynamic evaluation of licochalcone D. Results: Licochalcone D concentration-dependently inhibited Kv1.3 currents, with IC₅₀ values of 28.77 ± 3.40 nM in HEK293T cells and 497.72 ± 87.30 nM in Jurkat T cells. Ca²⁺ imaging revealed that it suppressed Ca²⁺ influx in T cells. Animal studies demonstrated that licochalcone D markedly improved psoriasiform lesions (erythema, scaling, thickening), reduced PASI scores and itching, alleviated epidermal hyperplasia and inflammatory infiltration, and down-regulated IL-6, IL-17, and IL-23 expression. Conclusion: Licochalcone D exerts immunomodulatory effects by blocking Kv1.3 channels, thereby alleviating psoriasiform skin inflammatory responses. This provides an experimental foundation and theoretical support for its potential as a targeted immunotherapy drug.

Published in	Science Discovery (Volume 13, Issue 6)
DOI	10.11648/j.sd.20251306.17
Page(s)	143-148
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2025. Published by Science Publishing Group

Keywords

Licochalcone D, Kv1.3 Channel, Psoriasis, T Cells, Immunomodulation

1．引言

银屑病（Psoriasis）是一种慢性、复发性、免疫介导的皮肤病，临床表现以红斑、鳞屑、表皮增厚及瘙痒为主，严重影响患者生活质量

[1, 2]

。近年研究表明，银屑病发病机制与T淋巴细胞异常激活密切相关，其中以IL-17和IL-23为主导的Th17通路在疾病发生与发展中起关键作用

[3-5]

。T细胞活化过程中，细胞内钙离子（Ca²⁺）信号的维持依赖于钾通道的调控功能，其中电压门控钾通道Kv1.3在效应记忆T细胞（TEM）中高表达，通过稳定膜电位和维持钙信号持续性，促进炎症因子释放及T细胞持续激活

[6]

。因此，Kv1.3通道被认为是银屑病等自身免疫性疾病的重要治疗靶点

[7]

。

甘草（Glycyrrhiza uralensis Fisch.）作为传统中药，具有清热解毒、抗炎等药理作用，其活性成分查尔酮类化合物近年来备受关注

[8, 9]

。已有研究报道，甘草查尔酮A具有一定免疫抑制活性

[10, 11]

，但关于其他查尔酮类化合物，特别是甘草查尔酮D（Licochalcone D，LCD）对Kv1.3通道的调控作用及其在T细胞相关疾病中的机制研究尚不充分。本研究以甘草查尔酮D为研究对象，采用全细胞膜片钳技术、钙成像及酶联免疫吸附试验（ELISA）等方法，系统评价其对Kv1.3通道及T细胞活化的影响，并通过咪喹莫特诱导的银屑病小鼠模型验证其体内治疗效果和抗炎机制，旨在为甘草查尔酮D作为靶向Kv1.3的小分子免疫调节剂在银屑病治疗中的应用提供实验依据。

2．材料与方法

2.1．材料

2.1.1．主要药品与试剂

甘草查尔酮D（纯度≥98%，成都埃法生物科技有限公司）；Fura-2 AM钙离子荧光探针（Beyotime）；Concanavalin A（ConA，上海源叶生物）；CCK-8检测试剂盒（Abbkine）；人IL-2 ELISA试剂盒（达科为）；胎牛血清、RPMI-1640培养基、青链霉素混合液（Gibco）；咪喹莫特乳膏（5%，四川明欣制药）；地塞米松磷酸钠注射液（布可敏）；其他常规试剂均为国产分析纯。

2.1.2．实验动物

SPF级C57BL/6雄性小鼠（8周龄），购自湖北省实验动物研究中心（许可证号：SYXK（鄂）2021-0089）。动物饲养于中南民族大学实验动物中心，恒温恒湿，12 h光/暗循环，自由摄食饮水。所有动物实验操作均遵循《实验动物管理条例》相关规定，并经本校动物实验伦理委员会批准（批准号：2025-SCUEC-077）。

2.1.3．细胞株

人T细胞白血病细胞系Jurkat T细胞和人胚胎肾细胞HEK293T细胞购自武汉普诺赛生物公司。Jurkat细胞培养于RPMI-1640培养基，HEK293T细胞培养于DMEM培养基，均补充10%胎牛血清和1%青链霉素混合液，37°C、5% CO₂条件下培养。

2.2．方法

2.2.1．Kv1.3电流的膜片钳检测

采用全细胞膜片钳技术记录甘草查尔酮D对Kv1.3通道的作用。将Kv1.3质粒瞬时转染入HEK293T细胞，24 h后进行记录。内液成分为（mmol/L）：KCl 140、MgCl₂ 1、EGTA 1、HEPES 10、Na₂ATP 3，pH 7.2；外液为NaCl 140、KCl 5、CaCl₂ 2、MgCl₂ 1、HEPES 10、Glucose 10，pH 7.4。膜电位钳制于−60 mV，每20 s给予400 ms、+50 mV的去极化脉冲。记录甘草查尔酮D不同浓度下对Kv1.3电流的抑制作用，并计算IC₅₀值。

2.2.2．T细胞Ca²⁺成像实验

使用Fura-2 AM染料标记Jurkat T细胞，采用倒置荧光显微镜监测细胞内游离Ca²⁺浓度变化。先用无钙外液冲洗细胞后，加入10 μM CPA诱导内质网钙释放，随后补加含2 mM Ca²⁺的HBSS溶液，观察细胞内Ca²⁺内流。分别记录在甘草查尔酮D作用前后的F340/F380荧光比值变化，分析其对钙离子内流的影响。

2.2.3．细胞活力检测

采用 CCK-8 试剂盒评估甘草查尔酮 D 的细胞安全性。

2.2.3．T细胞活化模型与IL-2释放检测

将Jurkat T细胞以1×10⁶个/孔接种于24孔板，加入50 μg/mL ConA刺激24 h，同时设定不同浓度甘草查尔酮D处理组（0.1、0.3、1、3、10 μM）和对照组。培养结束后收集上清液，采用ELISA法检测细胞分泌的IL-2水平。

2.2.4．小鼠银屑病模型建立与药物干预

将小鼠背部剃毛并脱毛，随机分为5组（n=6）：对照组、模型组（IMQ）、阳性对照组（地塞米松5 mg/kg）、LCD低剂量组（25 mg/kg）、LCD高剂量组（50 mg/kg）。除对照组外，其余各组于剃毛区连续7天每日外涂62.5 mg 5%咪喹莫特乳膏；对照组涂抹等量凡士林。自第4天起，药物干预组连续腹腔注射LCD或地塞米松，对照组和模型组注射等体积生理盐水，第7天解剖取材。

2.2.5．PASI评分及瘙痒行为观察

参照人PASI评分标准，分别对红斑、鳞屑、增厚三个指标评分（0~4分），取平均值作为PASI总分。抓挠行为采用红光环境下录像观察法，在第4天与第7天分别记录小鼠30 min内抓挠次数，并进行统计分析，所有评分均在双盲条件下完成。

2.2.6．皮肤组织病理及炎症因子检测

皮损组织经4%多聚甲醛固定、石蜡包埋、切片，HE染色后在光镜下观察皮肤结构变化。提取皮损组织总RNA，逆转录为cDNA后，采用实时荧光定量PCR检测IL-6、IL-17、IL-23的mRNA表达水平，以β-actin为内参，计算相对表达量。

2.2.7．脾脏指数测定

剖检后剥离小鼠脾脏，称重并计算脾脏指数（脾脏质量/体质量×100%），用于反映系统性免疫状态。

2.2.8．统计学分析

采用GraphPad Prism 9.0软件对实验结果进行统计分析及作图，实验数据以均数±标准误差（Mean±SEM）表示。各组数据在接受方差齐性检验后，采用t检验、单因素方差分析（ANOVA）进行统计学处理，当P<0.05表示差异有统计学意义。

3．实验结果

3.1．甘草查尔酮D对Kv1.3通道具有显著抑制作用

Kv1.3通道在T细胞功能调节中发挥重要作用，是近年来自身免疫性疾病研究中的关键靶点。为明确甘草查尔酮D对Kv1.3通道的调节作用，本研究采用全细胞膜片钳技术，分别在外源性表达Kv1.3的HEK293T细胞和内源性高表达Kv1.3的Jurkat T细胞中，检测甘草查尔酮D对Kv1.3电流的影响。在HEK293T细胞中转染Kv1.3质粒构建外源性表达模型后，给予不同浓度的甘草查尔酮D处理，记录Kv1.3通道电流的变化。结果显示，甘草查尔酮D可明显抑制Kv1.3电流，且呈浓度依赖性，浓度达到100 nM时即开始出现明显抑制效应，达500 nM以上时电流几乎被完全抑制。通过剂量-反应关系拟合曲线计算，甘草查尔酮D抑制外源性Kv1.3通道的IC₅₀值为28.77 ± 3.40 nM（图1A、B），提示其具有较强的通道电流抑制能力。为进一步验证其在免疫细胞中的作用，本研究在Jurkat T细胞中检测其对内源性Kv1.3通道的影响。实验结果同样显示，甘草查尔酮D能够显著抑制内源性Kv1.3电流，且在300 nM浓度下已出现明显抑制，呈典型的浓度依赖关系。其对Jurkat T细胞Kv1.3通道的IC₅₀值为497.72 ± 87.30 nM（图1C、D），较外源性表达系统略高，可能与细胞背景及通道构象差异有关。电生理实验结果表明甘草查尔酮D在外源性和内源性系统中均表现出显著的Kv1.3通道抑制活性，是一类具有明确靶点作用的小分子抑制剂，为后续免疫机制研究及动物模型验证提供了坚实的实验基础。

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图1 甘草查尔酮D对Kv1. .3电流的影响及浓度依赖曲线（n=5，Mean±SEM）。

（A）甘草查尔酮D对HEK293T细胞上Kv1.3通道电流的作用（B）甘草查尔酮D对HEK293T细胞上Kv1.3通道电流的浓度依赖曲线（C）甘草查尔酮D对Jurkat T细胞上Kv1.3通道电流的作用（D）甘草查尔酮D对Jurkat T细胞上Kv1.3通道电流的浓度依赖曲线

3.2．甘草查尔酮D抑制T细胞钙离子内流及IL-2释放

Kv1.3通道在T细胞活化过程中具有重要作用，尤其参与维持细胞膜电位与钙离子稳态。钙信号是T细胞介导免疫应答的核心环节，其持续性升高与炎症反应密切相关。为进一步探讨甘草查尔酮D对T细胞功能的调节作用，本研究采用钙成像技术和ELISA方法，观察其对Jurkat T细胞钙离子内流和细胞因子释放的影响。在钙成像实验中，使用Fura-2 AM荧光探针标记Jurkat T细胞后，记录细胞内游离Ca²⁺的荧光强度变化。实验结果显示，在细胞外补钙条件下，Ca²⁺浓度迅速上升，表现为F340/F380比值的明显增加。而在预处理1 μM甘草查尔酮D后，Ca²⁺内流的峰值显著下降（图2A、B），提示其有效抑制了细胞内钙离子浓度的升高。统计分析结果表明，LCD处理组F340/F380峰值比对照组下降约40%，差异具有统计学意义（P < 0.0001）（图2C）。为了进一步验证其对T细胞活化功能的影响，本研究采用ConA刺激Jurkat T细胞，建立体外T细胞活化模型，并在不同浓度甘草查尔酮D作用下检测IL-2的分泌水平。结果显示，甘草查尔酮D可在0.1~10 μM浓度范围内呈剂量依赖性抑制IL-2的释放（图2E）。其中，1 μM以上处理组的IL-2分泌水平较模型组显著降低（P < 0.0001），且在不影响细胞存活的前提下发挥免疫调节作用（图2D）。上述结果表明，甘草查尔酮D可通过抑制Kv1.3通道介导的钙内流，降低T细胞钙信号强度，并抑制炎症因子IL-2的释放。这一作用机制为其在银屑病等T细胞相关疾病中的应用提供了重要理论依据。

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Figure 2. 图2 甘草查尔酮D对Jurkat T细胞内Ca²⁺浓度及IL-2释放水平的影响。

（A）无药物处理时，Jurkat T细胞内Ca²⁺浓度变化（B）1µM 甘草查尔酮D处理后，Jurkat T细胞内Ca²⁺浓度变化 (C)1µM 甘草查尔酮D引起的Ca²⁺信号F340/F380的基线及变化值（D）甘草查尔酮D的对Jurkat T细胞的毒性影响（E)甘草查尔酮D对Jurkat T细胞IL-2释放水平的影响（ns：P＞0.05；**：P＜0.01；****：P＜0.0001）

3.3．甘草查尔酮D缓解银屑病小鼠皮肤炎症症状

为验证甘草查尔酮D在体内对银屑病样皮肤炎症的治疗效果，本研究采用咪喹莫特（Imiquimod, IMQ）诱导C57BL/6小鼠建立急性银屑病模型（图3A）。造模后小鼠背部皮肤表现出明显的红斑、鳞屑及增厚等典型银屑病样变化，同时伴随抓挠次数增加，提示皮肤瘙痒症状明显。实验分设模型组、阳性药物地塞米松组及甘草查尔酮D低、高剂量组（25 mg/kg、50 mg/kg），每天观察并评估小鼠皮肤症状变化情况。皮肤表型观察结果显示，IMQ模型组小鼠背部皮肤红斑、脱屑严重，表皮明显增厚；而甘草查尔酮D处理后，小鼠皮肤症状明显改善，红斑减轻，脱屑减少，表皮厚度也明显下降（图3B）。进一步对皮损区域进行红斑、鳞屑和增厚三项指标打分，并计算平均PASI评分，结果表明，甘草查尔酮D可显著降低小鼠PASI评分，尤其在50 mg/kg剂量下疗效更为显著（图3B，C）。此外，为评估皮肤炎症所致的瘙痒行为变化，对小鼠抓挠行为进行录像和统计。实验数据显示，IMQ模型组小鼠在造模第4天和第7天的单位时间抓挠次数明显高于对照组，而经甘草查尔酮D处理后，抓挠频率明显下降（图3D、E），与PASI评分改善趋势一致，提示其能有效缓解银屑病相关的瘙痒症状。甘草查尔酮D在IMQ诱导的银屑病小鼠模型中具有明显的皮肤症状改善作用，表现为皮损减轻、PASI评分下降及瘙痒行为减少，初步验证其体内抗银屑病效应。

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Figure 3. 图3 甘草查尔酮D缓解银屑病小鼠皮肤炎症症状（n=6，Mean±SEM）。

（A）构建小鼠银屑病模型（B）各组小鼠皮肤炎症情况（C）PASI指数变化示意图（D）治疗前各组小鼠抓挠次数统计图（E）治疗后各组小鼠抓挠次数统计图（ns：P＞0.05；**：P＜0.01；***：P＜0.001；****：P＜0.0001）

3.4．甘草查尔酮D改善银屑病小鼠皮肤病理病变并调控炎症因子表达

银屑病是一种以表皮角化过度、炎症细胞浸润及炎症因子异常表达为特征的慢性炎性皮肤病。为进一步验证甘草查尔酮D对银屑病小鼠皮损组织的改善作用，本研究对小鼠背部皮肤进行组织学及分子水平分析。HE染色结果显示，对照组小鼠皮肤组织结构正常，表皮较薄，角质层完整，细胞排列规则；而IMQ模型组小鼠皮肤表皮显著增厚，角化过度明显，伴有棘层不规则增生及大量炎症细胞浸润，提示银屑病样病变形成（图4A）。经甘草查尔酮D干预后，皮肤组织病理改变显著缓解，尤其在50 mg/kg剂量组中，表皮厚度下降，炎细胞浸润明显减少，角化现象亦较模型组有所改善（图4A），与阳性药物地塞米松组效果相近（图4A）。进一步通过实时荧光定量PCR检测银屑病相关炎症因子的表达水平，结果显示，IMQ模型组小鼠皮损组织中IL-6、IL-17和IL-23 mRNA表达水平均显著升高，而甘草查尔酮D处理后，上述炎症因子的表达明显下调，具有一定的剂量依赖性（图4C-E）。在50 mg/kg处理组中，三种因子的表达量均显著低于模型组（P < 0.01），提示其可有效抑制银屑病相关的炎症反应。此外，本研究还对各组小鼠的脾脏指数进行测定，以反映系统性免疫激活状态。结果发现，模型组小鼠脾脏指数显著高于对照组，而甘草查尔酮D治疗组脾脏指数明显下降（图4B），进一步支持其具有抑制异常免疫激活的作用。综上所述，甘草查尔酮D不仅能够显著改善银屑病小鼠皮肤组织结构异常，还能有效抑制局部及系统性炎症因子表达，从病理形态和分子机制两个层面验证了其治疗银屑病的潜力。

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图4 甘草查尔酮D改善银屑病小鼠皮损情况并调控炎症因子表达（n=6. .Mean±SEM）。

（A）各组小鼠皮损组织病理表现（HE，100×）（B）各组小鼠脾脏指数（C-E）各组小鼠皮肤组织中IL-6、IL-17、IL-23 mRNA的表达情况

4．讨论与结论

Kv1.3通道作为T细胞膜上关键的电压门控钾通道，在维持膜电位稳定和Ca²⁺内流持续性中发挥核心作用，直接影响T细胞活化、增殖及炎症因子分泌

[12,13]

。尤其在Th17等效应记忆T细胞中，Kv1.3高表达与银屑病、类风湿性关节炎等自身免疫性疾病的发生密切相关

[14,15]

。因此，靶向Kv1.3通道的小分子抑制剂成为治疗此类疾病的研究热点

[16]

。

本研究首次系统探讨了甘草查尔酮D对Kv1.3通道的抑制作用及其在银屑病样皮肤炎症模型中的治疗潜力。膜片钳实验结果表明，LCD高效抑制Kv1.3通道电流，在外源性表达系统中IC₅₀值为28.77 nM，显示出优异的靶点亲和力。相较于甘草查尔酮A等类似物，LCD在内源性T细胞模型中表现出更显著的抑制效果，提示其具有更高的生物学效能。进一步研究表明，LCD有效抑制T细胞内Ca²⁺内流，显著降低IL-2释放水平。IL-2作为T细胞活化的关键因子，其表达水平直接反映免疫细胞活性

[17, 18]

。LCD在不影响细胞存活率的前提下实现上述效应，表明其免疫抑制作用主要源于Kv1.3通道的功能阻断，而非非特异性细胞毒性。

体内实验结果显示，LCD显著改善咪喹莫特诱导的小鼠银屑病样皮肤损伤，表现为红斑、鳞屑和表皮增厚程度降低，银屑病面积与严重程度指数（PASI）评分及瘙痒行为显著改善。组织学分析（HE染色）进一步证实，LCD可有效抑制表皮过度增生及炎性细胞浸润，同时显著降低IL-6、IL-17和IL-23等关键炎症因子的表达

[19, 20]

。这些结果与LCD在体外对T细胞功能的抑制作用一致，提示其治疗银屑病的机制可能通过Kv1.3介导的T细胞通路调控实现。

与临床常用的糖皮质激素类药物相比，甘草查尔酮D来源于天然植物，结构明确，安全性较高，具备开发为新型免疫调节药物的潜力

[21]

。然而，LCD的药代动力学特性、长期毒性及临床转化潜力仍需进一步研究，以明确其在银屑病治疗中的应用前景。

本研究证实，甘草查尔酮D通过高效阻断Kv1.3通道，抑制T细胞Ca²⁺内流及IL-2释放，发挥显著的免疫抑制作用。在咪喹莫特诱导的银屑病小鼠模型中，LCD有效改善皮肤炎症症状，降低炎症因子表达，显示出良好的抗炎和免疫调节能力。本研究为甘草查尔酮D作为靶向Kv1.3的先导化合物提供了实验依据，为银屑病等T细胞介导性疾病的治疗提供了新思路。

作者基金

本文为国家自然科学基金资助项目(81373379，81641186)；湖北省自然科学基金创新发展联合基金重点项目（2024AFD262）和湖北省本科生创新创业训练计划（S202510524062）的阶段性成果之一。

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APA Style

Long, H., Xiang, Q., Lan, Z., Bai, L., Yin, S. (2025). Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Science Discovery, 13(6), 143-148. https://doi.org/10.11648/j.sd.20251306.17

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ACS Style

Long, H.; Xiang, Q.; Lan, Z.; Bai, L.; Yin, S. Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Sci. Discov. 2025, 13(6), 143-148. doi: 10.11648/j.sd.20251306.17

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AMA Style

Long H, Xiang Q, Lan Z, Bai L, Yin S. Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Sci Discov. 2025;13(6):143-148. doi: 10.11648/j.sd.20251306.17

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@article{10.11648/j.sd.20251306.17,
  author = {Haiqing Long and Qiu Xiang and Zhuxuan Lan and Luxiang Bai and Shijin Yin},
  title = {Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels
},
  journal = {Science Discovery},
  volume = {13},
  number = {6},
  pages = {143-148},
  doi = {10.11648/j.sd.20251306.17},
  url = {https://doi.org/10.11648/j.sd.20251306.17},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sd.20251306.17},
  abstract = {Objective: To investigate the blocking effect of licochalcone D on the voltage-gated potassium channel Kv1.3 and its potential therapeutic efficacy in psoriasiform skin inflammation, thereby providing experimental evidence for its use as an immunomodulatory candidate drug. Methods: The inhibitory effects of licochalcone D on exogenous and endogenous Kv1.3 currents were recorded by whole-cell patch-clamp. Ca2+ influx in Jurkat T cells was monitored with Fura-2 AM imaging. A ConA-induced T-cell activation model was established to quantify IL-2 secretion. An imiquimod-induced psoriasis-like mouse model was then established for in-vivo pharmacodynamic evaluation of licochalcone D. Results: Licochalcone D concentration-dependently inhibited Kv1.3 currents, with IC50 values of 28.77 ± 3.40 nM in HEK293T cells and 497.72 ± 87.30 nM in Jurkat T cells. Ca2+ imaging revealed that it suppressed Ca2+ influx in T cells. Animal studies demonstrated that licochalcone D markedly improved psoriasiform lesions (erythema, scaling, thickening), reduced PASI scores and itching, alleviated epidermal hyperplasia and inflammatory infiltration, and down-regulated IL-6, IL-17, and IL-23 expression. Conclusion: Licochalcone D exerts immunomodulatory effects by blocking Kv1.3 channels, thereby alleviating psoriasiform skin inflammatory responses. This provides an experimental foundation and theoretical support for its potential as a targeted immunotherapy drug.
},
 year = {2025}
}

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TY  - JOUR
T1  - Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels

AU  - Haiqing Long
AU  - Qiu Xiang
AU  - Zhuxuan Lan
AU  - Luxiang Bai
AU  - Shijin Yin
Y1  - 2025/12/24
PY  - 2025
N1  - https://doi.org/10.11648/j.sd.20251306.17
DO  - 10.11648/j.sd.20251306.17
T2  - Science Discovery
JF  - Science Discovery
JO  - Science Discovery
SP  - 143
EP  - 148
PB  - Science Publishing Group
SN  - 2331-0650
UR  - https://doi.org/10.11648/j.sd.20251306.17
AB  - Objective: To investigate the blocking effect of licochalcone D on the voltage-gated potassium channel Kv1.3 and its potential therapeutic efficacy in psoriasiform skin inflammation, thereby providing experimental evidence for its use as an immunomodulatory candidate drug. Methods: The inhibitory effects of licochalcone D on exogenous and endogenous Kv1.3 currents were recorded by whole-cell patch-clamp. Ca2+ influx in Jurkat T cells was monitored with Fura-2 AM imaging. A ConA-induced T-cell activation model was established to quantify IL-2 secretion. An imiquimod-induced psoriasis-like mouse model was then established for in-vivo pharmacodynamic evaluation of licochalcone D. Results: Licochalcone D concentration-dependently inhibited Kv1.3 currents, with IC50 values of 28.77 ± 3.40 nM in HEK293T cells and 497.72 ± 87.30 nM in Jurkat T cells. Ca2+ imaging revealed that it suppressed Ca2+ influx in T cells. Animal studies demonstrated that licochalcone D markedly improved psoriasiform lesions (erythema, scaling, thickening), reduced PASI scores and itching, alleviated epidermal hyperplasia and inflammatory infiltration, and down-regulated IL-6, IL-17, and IL-23 expression. Conclusion: Licochalcone D exerts immunomodulatory effects by blocking Kv1.3 channels, thereby alleviating psoriasiform skin inflammatory responses. This provides an experimental foundation and theoretical support for its potential as a targeted immunotherapy drug.

VL  - 13
IS  - 6
ER  -

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Haiqing Long

Ethnomedicine Level 3 Laboratory, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, China

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Qiu Xiang

Ethnomedicine Level 3 Laboratory, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, China

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Zhuxuan Lan

Ethnomedicine Level 3 Laboratory, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, China

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Luxiang Bai

Ethnomedicine Level 3 Laboratory, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, China

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Shijin Yin

Ethnomedicine Level 3 Laboratory, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, China

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Figure 图1 甘草查尔酮D对Kv1

图1 甘草查尔酮D对Kv1. .3电流的影响及浓度依赖曲线（n=5，Mean±SEM）。
Figure 2

Figure 2. 图 2 甘草查尔酮D对Jurkat T细胞内Ca²⁺浓度及IL-2释放水平的影响。
Figure 3

Figure 3. 图 3 甘草查尔酮D缓解银屑病小鼠皮肤炎症症状（n=6，Mean±SEM）。
Figure 图4 甘草查尔酮D改善银屑病小鼠皮损情况并调控炎症因子表达（n=6

图4 甘草查尔酮D改善银屑病小鼠皮损情况并调控炎症因子表达（n=6. .Mean±SEM）。

Plain Text BibTeX RIS

APA Style

Long, H., Xiang, Q., Lan, Z., Bai, L., Yin, S. (2025). Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Science Discovery, 13(6), 143-148. https://doi.org/10.11648/j.sd.20251306.17

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ACS Style

Long, H.; Xiang, Q.; Lan, Z.; Bai, L.; Yin, S. Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Sci. Discov. 2025, 13(6), 143-148. doi: 10.11648/j.sd.20251306.17

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AMA Style

Long H, Xiang Q, Lan Z, Bai L, Yin S. Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels. Sci Discov. 2025;13(6):143-148. doi: 10.11648/j.sd.20251306.17

Copy | Download

@article{10.11648/j.sd.20251306.17,
  author = {Haiqing Long and Qiu Xiang and Zhuxuan Lan and Luxiang Bai and Shijin Yin},
  title = {Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels
},
  journal = {Science Discovery},
  volume = {13},
  number = {6},
  pages = {143-148},
  doi = {10.11648/j.sd.20251306.17},
  url = {https://doi.org/10.11648/j.sd.20251306.17},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sd.20251306.17},
  abstract = {Objective: To investigate the blocking effect of licochalcone D on the voltage-gated potassium channel Kv1.3 and its potential therapeutic efficacy in psoriasiform skin inflammation, thereby providing experimental evidence for its use as an immunomodulatory candidate drug. Methods: The inhibitory effects of licochalcone D on exogenous and endogenous Kv1.3 currents were recorded by whole-cell patch-clamp. Ca2+ influx in Jurkat T cells was monitored with Fura-2 AM imaging. A ConA-induced T-cell activation model was established to quantify IL-2 secretion. An imiquimod-induced psoriasis-like mouse model was then established for in-vivo pharmacodynamic evaluation of licochalcone D. Results: Licochalcone D concentration-dependently inhibited Kv1.3 currents, with IC50 values of 28.77 ± 3.40 nM in HEK293T cells and 497.72 ± 87.30 nM in Jurkat T cells. Ca2+ imaging revealed that it suppressed Ca2+ influx in T cells. Animal studies demonstrated that licochalcone D markedly improved psoriasiform lesions (erythema, scaling, thickening), reduced PASI scores and itching, alleviated epidermal hyperplasia and inflammatory infiltration, and down-regulated IL-6, IL-17, and IL-23 expression. Conclusion: Licochalcone D exerts immunomodulatory effects by blocking Kv1.3 channels, thereby alleviating psoriasiform skin inflammatory responses. This provides an experimental foundation and theoretical support for its potential as a targeted immunotherapy drug.
},
 year = {2025}
}

Copy | Download

TY  - JOUR
T1  - Licochalcone D Alleviates Psoriasiform Skin Inflammation by Inhibiting Kv1.3 Channels

AU  - Haiqing Long
AU  - Qiu Xiang
AU  - Zhuxuan Lan
AU  - Luxiang Bai
AU  - Shijin Yin
Y1  - 2025/12/24
PY  - 2025
N1  - https://doi.org/10.11648/j.sd.20251306.17
DO  - 10.11648/j.sd.20251306.17
T2  - Science Discovery
JF  - Science Discovery
JO  - Science Discovery
SP  - 143
EP  - 148
PB  - Science Publishing Group
SN  - 2331-0650
UR  - https://doi.org/10.11648/j.sd.20251306.17
AB  - Objective: To investigate the blocking effect of licochalcone D on the voltage-gated potassium channel Kv1.3 and its potential therapeutic efficacy in psoriasiform skin inflammation, thereby providing experimental evidence for its use as an immunomodulatory candidate drug. Methods: The inhibitory effects of licochalcone D on exogenous and endogenous Kv1.3 currents were recorded by whole-cell patch-clamp. Ca2+ influx in Jurkat T cells was monitored with Fura-2 AM imaging. A ConA-induced T-cell activation model was established to quantify IL-2 secretion. An imiquimod-induced psoriasis-like mouse model was then established for in-vivo pharmacodynamic evaluation of licochalcone D. Results: Licochalcone D concentration-dependently inhibited Kv1.3 currents, with IC50 values of 28.77 ± 3.40 nM in HEK293T cells and 497.72 ± 87.30 nM in Jurkat T cells. Ca2+ imaging revealed that it suppressed Ca2+ influx in T cells. Animal studies demonstrated that licochalcone D markedly improved psoriasiform lesions (erythema, scaling, thickening), reduced PASI scores and itching, alleviated epidermal hyperplasia and inflammatory infiltration, and down-regulated IL-6, IL-17, and IL-23 expression. Conclusion: Licochalcone D exerts immunomodulatory effects by blocking Kv1.3 channels, thereby alleviating psoriasiform skin inflammatory responses. This provides an experimental foundation and theoretical support for its potential as a targeted immunotherapy drug.

VL  - 13
IS  - 6
ER  -

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