@article{Liu2026, 
author = {Miao-Miao Liu and Jie Bai and Zi-Ye Tian and Ting-Ting Zheng and Teun Boekhout and Qi-Ming Wang},
title = {Oxymatrine ameliorates Malassezia overgrowth-induced psoriasis in vivo and in vitro by inhibiting the biofilm formation and inflammation},
year = {2026},
journal = {Mycology},
volume = {17},
number = {1},
pages = {196-216},
keywords = {Oxymatrine, Malassezia, psoriasis, biofilm, inflammation},
url = {https://www.sciopen.com/article/10.1080/21501203.2025.2511903},
doi = {10.1080/21501203.2025.2511903},
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.}
}