# Oxymatrine ameliorates Malassezia overgrowth-induced psoriasis in vivo and in vitro by inhibiting the biofilm formation and inflammation

**Authors:** Miao-Miao Liu, Jie Bai, Zi-Ye Tian, Ting-Ting Zheng, Teun Boekhout, Qi-Ming Wang

PMC · DOI: 10.1080/21501203.2025.2511903 · Mycology · 2025-06-10

## TL;DR

Oxymatrine reduces Malassezia-related psoriasis by inhibiting biofilm formation and inflammation in both lab and animal models.

## Contribution

Oxymatrine's therapeutic potential against Malassezia-associated psoriasis is demonstrated for the first time.

## Key findings

- Oxymatrine reduces Malassezia biofilm formation at 0.64 mg/mL.
- Oxymatrine alleviates psoriatic lesions and improves skin barrier integrity.
- Oxymatrine modulates oxidative stress and inflammation via STAT3/Nf-κB and AhR/Nrf2 pathways.

## Abstract

The basidiomycetous yeast genus Malassezia is involved in the exacerbation of psoriatic lesions. Oxymatrine (OMT), a quinoline alkaloid derived from Sophora flavescens, exhibits diverse pharmacological properties, including anti-inflammatory, anticancer, and antiviral effects. However, whether OMT exerts therapeutic effects against Malassezia-associated psoriasis remains unclear. This work aimed to study the antifungal and antibiofilm effect of OMT on several Malassezia species and the therapeutic benefits of OMT on Malassezia-associated psoriasis in vivo and in vitro. Treatment with 0.64 mg/mL OMT showed decreasing levels of biofilm formation of Malassezia species. Histomorphology and functional analyses demonstrated that OMT treatment effectively alleviated Malassezia-induced psoriatic lesions and repaired skin barrier integrity. Furthermore, the results demonstrate that OMT significantly reduced the levels of malonaldehyde, interleukin (IL)-6, IL-17, IL-23, and tumour necrosis factor (TNF)-α while promoting the activation of superoxide dismutase, catalase, and glutathione. OMT also reversed Malassezia-associated apoptosis and decreased the expression of the STAT3/Nf-κB/p-Nf-κB signalling pathway. Additionally, OMT reduces the nuclear expression of AhR/Nrf2 in Malassezia-stimulated HaCaT cells. In summary, this study demonstrated that OMT inhibits Malassezia biofilm formation and ameliorates Malassezia-associated psoriasis by modulating oxidative stress, inflammation, and apoptosis via STAT3/Nf-κB and AhR/Nrf2 pathways.

## Linked entities

- **Proteins:** STAT3 (signal transducer and activator of transcription 3), NFKB1 (nuclear factor kappa B subunit 1), AHR (aryl hydrocarbon receptor), GABPA (GA binding protein transcription factor subunit alpha)
- **Chemicals:** Oxymatrine (PubChem CID 114850), malonaldehyde (PubChem CID 10964), glutathione (PubChem CID 124886)
- **Diseases:** psoriasis (MONDO:0005083)
- **Species:** Malassezia (taxon 55193)

## Full-text entities

- **Genes:** NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CAT (catalase) [NCBI Gene 847], AHR (aryl hydrocarbon receptor) [NCBI Gene 196] {aka FVH3, RP85, bHLHe76}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}
- **Diseases:** inflammation (MESH:D007249), Malassezia (MESH:D014010), psoriatic lesions (MESH:D015535), psoriasis (MESH:D011565)
- **Chemicals:** glutathione (MESH:D005978), quinoline alkaloid (-), malonaldehyde (MESH:D008315), OMT (MESH:C037573)
- **Species:** Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Malassezia (genus) [taxon 55193], Sophora flavescens (species) [taxon 49840]

## Full text

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## Figures

25 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13007419/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC13007419/full.md

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Source: https://tomesphere.com/paper/PMC13007419