Cutaneous and ocular toxicology · 2025
Therapeutic effect of systemic use of glatiramer acetate in imiquimod-induced mouse psoriasis model.
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Demiran Goknur, Guner Rukiye Yasak, Ozkara Mustafa, Tosun Mustafa, Akyol Melih
Аннотация
PURPOSE: The aim of this study is to evaluate the therapeutic potential of systemic glatiramer acetate (GA), a drug used in the treatment of multiple sclerosis (MS), in an imiquimod-induced psoriasis mouse model, given the common immunopathogenic mechanisms between the two diseases.
MATERIALS AND METHODS: Fifty-four adult female BALB/c mice (16-18 weeks old) were divided into nine groups (6 mice each). A psoriasis-like model was induced in eight groups by application of 5% imiquimod cream for seven days. Systemic treatments included methotrexate (2 mg/kg/week), saline (1 mL/kg/day) and GA at doses ranging from 50 to 100 mcg, administered subcutaneously either during or after the induction phase. Clinical severity was assessed using the modified Psoriasis Area and Severity Index (mPASI), while histopathological and immunohistochemical analyses were performed to assess inflammation and cytokine expression, focusing on TNF-α, IL-1β and IL-17.
RESULTS: The highest mPASI scores were observed in the untreated psoriasis group, whereas the healthy control and mice treated with 50 mcg GA, especially after induction, showed the lowest scores. Statistically significant improvements in histopathological scores were observed (p < 0.05). GA treatment at 50 mcg resulted in the most favourable cytokine profile, with TNF-α and IL-17 levels comparable to the healthy group and a similar trend observed for IL-1β expression.
CONCLUSIONS: Among the doses tested, 50 mcg GA administered after model induction was the most effective in reducing clinical severity and inflammatory cytokine expression. These findings suggest that GA is a promising systemic therapeutic agent for psoriasis.
MATERIALS AND METHODS: Fifty-four adult female BALB/c mice (16-18 weeks old) were divided into nine groups (6 mice each). A psoriasis-like model was induced in eight groups by application of 5% imiquimod cream for seven days. Systemic treatments included methotrexate (2 mg/kg/week), saline (1 mL/kg/day) and GA at doses ranging from 50 to 100 mcg, administered subcutaneously either during or after the induction phase. Clinical severity was assessed using the modified Psoriasis Area and Severity Index (mPASI), while histopathological and immunohistochemical analyses were performed to assess inflammation and cytokine expression, focusing on TNF-α, IL-1β and IL-17.
RESULTS: The highest mPASI scores were observed in the untreated psoriasis group, whereas the healthy control and mice treated with 50 mcg GA, especially after induction, showed the lowest scores. Statistically significant improvements in histopathological scores were observed (p < 0.05). GA treatment at 50 mcg resulted in the most favourable cytokine profile, with TNF-α and IL-17 levels comparable to the healthy group and a similar trend observed for IL-1β expression.
CONCLUSIONS: Among the doses tested, 50 mcg GA administered after model induction was the most effective in reducing clinical severity and inflammatory cytokine expression. These findings suggest that GA is a promising systemic therapeutic agent for psoriasis.