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Research
Chang-Hyun Kim
Dongguk University College of Medicine
Corresponding Author
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Background: Psoriasis is a chronic and relapsing inflammatory autoimmune skin disease. We recently reported that SC-E1 has various beneficial biological effects, including anti-inflammatory activity in an in vitro experimental study. Therefore, SC-E1 has been expected as complementary and alternative medicines for various inflammatory autoimmune skin diseases, including psoriasis. In this study, we investigated the potential anti-psoriatic effect of SC-E1 using an imiquimod (IMQ)-induced skin inflammation in mice and explored the mechanism underlying those actions.
Methods: Psoriatic dermatitis was induced by repeated challenges with IMQ on the backs of C57BL/6 mice. SC-E1 (250 mg/kg, 500 mg/kg, and 1000 mg/kg) was administered to the mice orally once a day by oral gavage needle for 5 days before and together with IMQ application for another 7 days (totally 12 days of treatment). The anti-psoriatic effects of SC-E1 were evaluated by dermatitis score, skin histology, and immunological parameters. In addition, the mechanisms responsible for the immunomodulatory effect of SC-E1 were examined using p38 MAPK, IκBα, and NF-κB.
Results: We found that SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment ameliorated the development of IMQ-induced skin inflammation in mice. Histological analysis revealed a reduction of epidermal thickening, hyperkeratosis, and inflammatory cell infiltration in SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment. Moreover, SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment effectively attenuated production of Th1 cytokines (TNF-a, IFN-g) and Th17 cytokines (IL-17A and IL-23) in the serum and dorsal skin induced by IMQ in mice. SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment also inhibited splenomegaly. In addition, SC-E1 inhibited the expression of inflammatory modulators, such as p38 MAPK, IκBα, and NF-κB in the skin of mice induced by IMQ.
Conclusion: Our present study demonstrated that the immunomodulatory mechanism underlying the anti-psoriatic effect of SC-E1 on IMQ-induced in mice may be attributed to the inhibition of production of various systemic proinflammatory mediators via a mechanism that may involve the inhibition of MAPK and NF-κB signaling pathway. Based on the results we suggest that SC-E1 could be considered as an anti-psoriatic agent for the prevention or treatment of inflammatory autoimmune skin diseases including psoriasis.
Keywords
SC-E1, Psoriasis, Imiquimod, Immunomodulation, Inflammatory mediators
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This is a preprint. It has not completed peer review.
Research
Chang-Hyun Kim
Dongguk University College of Medicine
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 02 Jun, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Biotechnology and Bioengineering
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Psoriasis is a chronic and relapsing inflammatory autoimmune skin disease. We recently reported that SC-E1 has various beneficial biological effects, including anti-inflammatory activity in an in vitro experimental study. Therefore, SC-E1 has been expected as complementary and alternative medicines for various inflammatory autoimmune skin diseases, including psoriasis. In this study, we investigated the potential anti-psoriatic effect of SC-E1 using an imiquimod (IMQ)-induced skin inflammation in mice and explored the mechanism underlying those actions.
Methods: Psoriatic dermatitis was induced by repeated challenges with IMQ on the backs of C57BL/6 mice. SC-E1 (250 mg/kg, 500 mg/kg, and 1000 mg/kg) was administered to the mice orally once a day by oral gavage needle for 5 days before and together with IMQ application for another 7 days (totally 12 days of treatment). The anti-psoriatic effects of SC-E1 were evaluated by dermatitis score, skin histology, and immunological parameters. In addition, the mechanisms responsible for the immunomodulatory effect of SC-E1 were examined using p38 MAPK, IκBα, and NF-κB.
Results: We found that SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment ameliorated the development of IMQ-induced skin inflammation in mice. Histological analysis revealed a reduction of epidermal thickening, hyperkeratosis, and inflammatory cell infiltration in SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment. Moreover, SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment effectively attenuated production of Th1 cytokines (TNF-a, IFN-g) and Th17 cytokines (IL-17A and IL-23) in the serum and dorsal skin induced by IMQ in mice. SC-E1 (500 mg/kg) or SC-E1 (1000 mg/kg) pretreatment also inhibited splenomegaly. In addition, SC-E1 inhibited the expression of inflammatory modulators, such as p38 MAPK, IκBα, and NF-κB in the skin of mice induced by IMQ.
Conclusion: Our present study demonstrated that the immunomodulatory mechanism underlying the anti-psoriatic effect of SC-E1 on IMQ-induced in mice may be attributed to the inhibition of production of various systemic proinflammatory mediators via a mechanism that may involve the inhibition of MAPK and NF-κB signaling pathway. Based on the results we suggest that SC-E1 could be considered as an anti-psoriatic agent for the prevention or treatment of inflammatory autoimmune skin diseases including psoriasis.
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