# Sinhyotaklisan as a Potential Therapeutic for Psoriasis: Network Pharmacology and Experimental Validation

**Authors:** Jung-Yun Ahn, Dong-Woo Lim, Jin-Hee Kim, Sung-Yun Park, Sun-Dong Park, Ju-Hee Lee

PMC · DOI: 10.3390/ijms26115082 · 2025-05-25

## TL;DR

This study explores how a traditional herbal formula called Sinhyotaklisan may help treat psoriasis by reducing inflammation and abnormal skin cell growth.

## Contribution

The study identifies Sinhyotaklisan's potential as a new treatment for psoriasis through network pharmacology and experimental validation.

## Key findings

- SHTLS suppressed TNF-α-induced VEGF and HIF-1α expression while upregulating p53 in HaCaT cells.
- SHTLS reduced IL-6 and IL-8 levels and inhibited NF-κB and MAPK pathways in vitro.
- In vivo, SHTLS alleviated psoriatic lesions in an imiquimod-induced mouse model.

## Abstract

Sinhyotaklisan (SHTLS) is a traditional herbal prescription composed of Lonicerae Flos, Angelicae Gigantis Radix, Astragali Radix, and Glycyrrhizae Radix et Rhizoma, commonly used to treat skin disorders. This study aimed to investigate the therapeutic effects and underlying mechanisms of SHTLS in psoriasis through the network pharmacology analysis and experimental validation in vitro and in vivo. Bioactive compounds and molecular targets were identified using the Traditional Chinese Medicine Systems Pharmacology database, and key protein–protein interaction networks were analyzed via STRING and Cytoscape. In vitro, HaCaT cells were pretreated with SHTLS and stimulated with TNF-α, followed by assessments using proliferation assays, scratch assays, quantitative real-time PCR, and Western blotting. In vivo, the anti-psoriatic effects of SHTLS were evaluated in an imiquimod-induced psoriatic mouse model. A total of 36 key targets were significantly enriched in TNF-α, MAPK, HIF-1α, and IL-17 signaling pathways. SHTLS suppressed TNF-α-induced expression of VEGF and HIF-1α, while upregulating p53, thereby inhibiting keratinocyte hyperproliferation and angiogenesis. It also reduced IL-6 and IL-8 levels and blocked activation of the NF-κB and MAPK pathways. Histological analysis confirmed that SHTLS alleviated psoriatic lesions in vivo. These findings suggest that SHTLS may be a promising therapeutic candidate for psoriasis by targeting hyperproliferation, angiogenesis, and inflammation.

## Linked entities

- **Genes:** VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422], HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091], TP53 (tumor protein p53) [NCBI Gene 7157], IL6 (interleukin 6) [NCBI Gene 3569], CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790]
- **Diseases:** psoriasis (MONDO:0005083)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091] {aka HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}
- **Diseases:** psoriatic (MESH:D015535), inflammation (MESH:D007249), skin disorders (MESH:D012871), Psoriasis (MESH:D011565)
- **Chemicals:** imiquimod (MESH:D000077271), Angelicae Gigantis Radix (-)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]
- **Cell lines:** HaCaT — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0038)

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12155304/full.md

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Source: https://tomesphere.com/paper/PMC12155304