Could Euphorbia neriifolia help with psoriasis

[Fred]

Pphytoconstituents of Euphorbia neriifolia exhibit stronger binding affinities toward the receptor protein 5hi4 (macrocyclic IL-17A antagonist) compared to the standard anti-psoriatic drugs Methotrexate and Apremilast.

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Psoriasis is a chronic autoimmune skin disorder characterized by persistent inflammation and excessive keratinocyte proliferation. Although conventional immunosuppressive therapies are clinically effective, their long-term use is often associated with adverse side effects, highlighting the need for safer alternative treatments.

Euphorbia neriifolia, a traditional medicinal plant known for its anti-inflammatory properties, has been investigated for its potential anti-psoriatic activity. In the present study, molecular docking was performed to evaluate the binding affinities of key phytoconstituents from E. neriifolia against interleukin-17A (IL-17A; PDB ID: 5HI4), a major cytokine implicated in psoriasis pathogenesis.

Docking analysis revealed that compounds such as Taraxerol, Glutinol acetate, and Epifriedelanol showed the highest binding affinities, with scores of −10.3, −10.0, and −10.0 kcal/mol, respectively, surpassing the reference drug methotrexate (−9.2 kcal/mol). Density functional theory (DFT) calculations further supported the electronic stability and reactivity of the top-ranked compounds, indicating their potential suitability as bioactive leads.

The integration of docking and DFT results highlights the novelty of this study, as E. neriifolia phytochemicals have not been extensively explored against IL-17A compared to other medicinal plants studied for psoriasis. The in vitro biological activity of the plant extract was also evaluated by using the L929 fibroblast bioassay, and the IC50 value was found to be 168.18 μg/mL.

Overall, the findings suggest that selected phytochemicals from E. neriifolia exhibit promising interactions with IL-17A, supporting their possible therapeutic role in psoriasis. These findings support further mechanistic and in vivo studies to validate IL-17A inhibition.

Source: onlinelibrary.wiley.com

*Funding: No funding reported