Kaempferol attenuates imiquimod-induced psoriatic skin inflammation in a mouse model. - GreenMedInfo Summary
Kaempferol attenuates imiquimod-induced psoriatic skin inflammation in a mouse model.
Clin Exp Immunol. 2019 Aug 13. Epub 2019 Aug 13. PMID: 31407330
Cuihua Liu
Psoriasis is an immune-mediated inflammatory skin disease that mainly affects the skin barrier. Treatment for psoriasis mainly includes conventional immunosuppressive drugs. However, long-term treatment with global immunosuppressive agents may cause a variety of side effects, including nephrotoxicity and infections. Kaempferol, a natural flavonol present in various plants, is known to possess potent anti-inflammatory, antioxidant and anti-cancerous properties. However, it's unknown whether kaempferol is also anti-psoriatic. Here we established an imiquimod (IMQ)-induced psoriatic mouse model to explore the potential therapeutic effects of kaempferol on psoriatic skin lesion and inflammation. In this study, we demonstrated that treatment with kaempferol protected mice from developing psoriasis-like skin lesion induced by topical administration of IMQ. Kaempferol reduced CD3T cell infiltration and gene expression of major proinflammatory cytokines, including IL-6, IL-17A and TNFα, in the psoriatic skin lesion. It also down-regulated proinflammatory NFκB signaling in the skin. The therapeutic effects were associated with a significant increase in CD4FoxP3Treg frequency in the spleen and lymph nodes as well as FoxP3-positive staining in the skin lesion. On the other hand, depletion of CD4CD25Tregs reversed the therapeutic effects of kaempferol on the skin lesion. Kaempferol also lowered the percentage of IL17ACD4T cells in the spleen and lymph nodes of IMQ-induced psoriatic mice. Finally, kaempferol suppressed the proliferation of T cells in vitro and their mTOR signaling as well. Thus, our findings suggest that kaempferol may be a therapeutic drug for treating human psoriasis in the near future. This article is protected by copyright. All rights reserved.