Exploring the therapeutic potential of Abelmoschi Corolla in psoriasis: Mechanisms of action and inflammatory pathway disruption

Abstract

Background

Psoriasis is a prevalent chronic inflammatory skin condition for which existing treatments often fall short of fully addressing patient needs. Abelmoschi Corolla (AC), a traditional Chinese medicine, and its ethanol extract, huangkui capsule, are well established for the treatment of chronic kidney diseases. The therapeutic mechanisms of AC include anti-inflammatory effects and immune modulation, which align with psoriasis treatment strategies. Nevertheless, the potential of AC as a therapeutic agent for psoriasis remains unexplored.

Purpose

This study aimed to evaluate the efficacy of AC in treating psoriasis and, if effective, to elucidate the underlying mechanisms by which AC exerts its therapeutic effects.

Methods

To assess the therapeutic potential of AC, an imiquimod-induced psoriasis-like mouse model was utilized. Bioinformatics and machine learning approaches were employed to predict the targets and mechanisms of AC in psoriasis. Further validation was performed using targeted metabolite quantification, immunohistochemistry, polymerase chain reaction, and western blotting.

Results

AC treatment significantly improved psoriasis-like skin lesions, as indicated by enhancements in appearance, PASI scores, a reduction in epidermal hyperproliferation, and decreased immune cell infiltration. Bioinformatics and machine learning analyses identified arginase 1 (ARG1) as a key target of AC in psoriasis. Experimental validation demonstrated that AC reduced ARG1 expression, arginine metabolism, and polyamine production by upregulating PP6 expression and inhibiting C/EBP-β activation in psoriatic keratinocytes, resulting in the suppression of dendritic cell infiltration and a reduction in the expression of inflammatory cytokines, including IL-23, IL-6, IL-1β, IL-17A, and TNF-α.

Conclusions

AC disrupted the inflammatory pathways associated with psoriasis and alleviated imiquimod-induced psoriasis-like skin inflammation by inhibiting ARG1 overexpression and arginine metabolism in psoriatic keratinocytes. These findings suggest that AC has significant potential as a therapeutic agent for psoriasis and warrants further research and development.