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

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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

References

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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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Author Information

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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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}
}

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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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