# Investigation of the mechanism of Xiaoyin Jiedu Yin in the treatment of psoriasis based on bioinformatics, machine learning

**Authors:** Ru-Nan Fang, Yang Zhou, Yang Shen, Yuan Sun, Jian-Hong Li

PMC · DOI: 10.3389/fchem.2025.1623449 · 2025-07-15

## TL;DR

This study explores how a traditional Chinese medicine, Xiaoyin Jiedu Yin, treats psoriasis by identifying a key protein target and validating its effects using advanced techniques.

## Contribution

The study identifies AKR1B10 as a core therapeutic target of Xiaoyin Jiedu Yin in psoriasis treatment using bioinformatics and experimental validation.

## Key findings

- AKR1B10 is upregulated in psoriatic lesions and linked to inflammatory immune cells.
- XYJDY reduces AKR1B10 expression in IL-17A–stimulated HaCaT cells.
- The formula acts via a multi-target mechanism to treat psoriasis.

## Abstract

Psoriasis is a chronic immune-mediated inflammatory skin disease. Xiaoyin Jiedu Decoction (XYJDY) is a traditional Chinese medicinal formula that has demonstrated significant clinical efficacy in alleviating psoriatic symptoms; however, its underlying pharmacological mechanisms remain unclear.

We employed network pharmacology, machine learning–based target screening, and functional enrichment to identify key targets and pathways. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) were used to validate gene expression. An IL-17A–induced HaCaT cell model was established for in vitro validation.

AKR1B10 was identified as the core therapeutic target of XYJDY in psoriasis. It was markedly upregulated in psoriatic skin lesions, primarily enriched in keratinocytes, and its expression demonstrated positive correlations with multiple pro-inflammatory immune cell subsets. In vitro experiments showed that XYJDY-medicated serum significantly downregulated AKR1B10 expression in IL–17A–stimulated HaCaT cells.

This study reveals that the multi-component formula XYJDY exerts anti-psoriatic effects through a multi-target synergistic mechanism, in which AKR1B10 is a potential core target. These findings provide a theoretical foundation for further exploration of the molecular mechanisms underlying the efficacy of XYJDY in psoriasis treatment.

## Linked entities

- **Genes:** AKR1B10 (aldo-keto reductase family 1 member B10) [NCBI Gene 57016], IL17A (interleukin 17A) [NCBI Gene 3605]
- **Diseases:** psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** CXCL13 (C-X-C motif chemokine ligand 13) [NCBI Gene 10563] {aka ANGIE, ANGIE2, BCA-1, BCA1, BLC, BLR1L}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, IRAK1 (interleukin 1 receptor associated kinase 1) [NCBI Gene 3654] {aka IRAK, pelle}, CXCR2 (C-X-C motif chemokine receptor 2) [NCBI Gene 3579] {aka CD182, CDw128b, CMKAR2, IL8R2, IL8RA, IL8RB}, CXCR6 (C-X-C motif chemokine receptor 6) [NCBI Gene 10663] {aka BONZO, CD186, CDw186, STRL33, TYMSTR}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, Il17a (interleukin 17A) [NCBI Gene 301289] {aka CTLA-8, IL-17, IL-17A, Il17}, VN1R17P (vomeronasal 1 receptor 17 pseudogene) [NCBI Gene 441931] {aka GPCR}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, CXCL1 (C-X-C motif chemokine ligand 1) [NCBI Gene 2919] {aka FSP, GRO1, GROa, MGSA, MGSA-a, NAP-3}, MMP3 (matrix metallopeptidase 3) [NCBI Gene 4314] {aka CHDS6, MMP-3, SL-1, STMY, STMY1, STR1}, KEAP1 (kelch like ECH associated protein 1) [NCBI Gene 9817] {aka INrf2, KLHL19}, Akr1b10 (aldo-keto reductase family 1 member B10) [NCBI Gene 296972], AKR1B10 (aldo-keto reductase family 1 member B10) [NCBI Gene 57016] {aka AKR1B11, AKR1B12, ALDRLn, ARL-1, ARL1, HIS}, LEPR (leptin receptor) [NCBI Gene 3953] {aka CD295, LEP-R, LEPRD, OB-R, OBR, huB219}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, CCL20 (C-C motif chemokine ligand 20) [NCBI Gene 6364] {aka CKb4, Exodus, LARC, MIP-3-alpha, MIP-3a, MIP3A}, AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, CCR7 (C-C motif chemokine receptor 7) [NCBI Gene 1236] {aka BLR2, CC-CKR-7, CCR-7, CD197, CDw197, CMKBR7}, BCL2A1 (BCL2 related protein A1) [NCBI Gene 597] {aka ACC-1, ACC-2, ACC1, ACC2, BCL2L5, BFL1}, EGF (epidermal growth factor) [NCBI Gene 1950] {aka HOMG4, URG}, XDH (xanthine dehydrogenase) [NCBI Gene 7498] {aka XAN1, XDH/XO, XO, XOR}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, POTEF (POTE ankyrin domain family member F) [NCBI Gene 728378] {aka A26C1B, POTE2alpha, POTEACTIN}
- **Diseases:** plaque (MESH:D003773), inflammatory arthritis (MESH:D001168), psoriatic (MESH:D015535), inflammatory skin disease (MESH:D012871), cardiometabolic disorders (MESH:D024821), blood stasis (MESH:D014647), inflammation (MESH:D007249), autoimmune dysregulation (MESH:C580192), Psoriasis (MESH:D011565), gastrointestinal diseases (MESH:D005767), HL (MESH:C538324), toxicity (MESH:D064420)
- **Chemicals:** penicillin (MESH:D010406), PMSF (MESH:D010664), water (MESH:D014867), PVDF (MESH:C024865), lipopolysaccharide (MESH:D008070), lipid (MESH:D008055), NO (MESH:D009614), S (MESH:D013455), SDS (MESH:D012967), CO2 (MESH:D002245), P (MESH:D010758), CCK-8 (-), isoflurane (MESH:D007530), streptomycin (MESH:D013307)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Paris (genus) [taxon 49669], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** AUC of 0, C-26 C
- **Cell lines:** -2410- — Bos taurus (Bovine), Finite cell line (CVCL_A2KJ), HaCaT — Homo sapiens (Human), Spontaneously immortalized cell line (CVCL_0038)

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12303907/full.md

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Source: https://tomesphere.com/paper/PMC12303907