EXPERIMENTAL RESEARCH
Oleuropein modulates over-proliferation of keratinocytes in mice with imiquimodmediated psoriasis and inhibits differentiation of TH17 cells through the JAK3/STAT3 axis
Quan Shi 1, 2,   Qi He 1, 2,   Weiming Chen 1, 2,   Jianwen Long 1, 2,   Bo Zhang 1, 2
 
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1
Department of Dermatology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei, China
2
Department of Dermatology, Hubei Province Academy of Traditional Chinese Medicine, Wuhan, Hubei, China
Submission date: 2020-08-07
Final revision date: 2020-08-28
Acceptance date: 2020-09-11
Online publication date: 2020-11-06
 
 
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ABSTRACT
Introduction:
Oleuropein (OLP) is polyphenol obtained from olive oil; it is proved in Chinese traditional medicine for its use in disorders including autoimmune and inflammatory disorders. Psoriasis (PSR) is an autoimmune and inflammatory disorder triggered by T-helper-17 (Th17) cells.

Material and methods:
We developed an imiquimod (IMQ)-mediated PSR model in mice to study the anti-inflammatory role of OLP in psoriasis. The mice were given 50 mg/kg and 100 mg/kg dose of OLP. Histology was done to assess the inflammation of lesions. Western blot analysis was done for JAK3/STAT3 in isolated T cells, expression of RORgt was done by RT-PCR. The In silico molecular docking studies were done for interaction of OLP with target protein STAT3 and JAK3.

Results:
Treatment of OLP attenuated proliferation in IMQ-mediated keratinocytes, improved infiltration of CD3+ cells in the skin lesions and in CD4+ and CD8+ T cells and also ameliorated the levels of cytokines. In in vitro studies in isolated T cells, OLP blocked the differentiation of Th17 cells and also the levels of IL-17 and the JAK3/STAT3 pathway. The in silico docking showed that OLP had potential binding affinity with JAK3 and STAT3 which was parallel to in vivo and in vitro findings.

Conclusions:
OLP ameliorates psoriasis skin lesions by blocking Th17-mediated inflammation. OLP may be an interesting molecule for treating autoimmunity in psoriasis.

eISSN:1896-9151
ISSN:1734-1922