Abstract
Psoriasis is a chronic inflammatory skin condition characterized by abnormal keratinocyte proliferation and differentiation that is accompanied with dysregulated immune response and abnormal vascularization. Devil’s claw (Harpagophytum procumbens (Burch.) DC. ex Meisn.) tubers extract has been used both systemically and topically for treatment of chronic inflammatory diseases such as arthritis, osteoporosis, inflammatory bowel disease, among others. However, its potential mechanisms of action against psoriasis remains poorly investigated. The human keratinocyte HaCaT cell line is a well-accepted in vitro model system for inflammatory skin disorders such as psoriasis. The present study involved an exploration of the effect of biotechnologically produced H. procumbens (HP) cell suspension extract and pure phenylethanoid glycosides verbascoside (VER) and leucosceptoside A (LEU) in interferon (IFN)-γ/interleukin (IL)-17A/IL-22-stimulated HaCaT cells as a model of psoriasis-like inflammation. Changes in key inflammatory signaling pathways related to psoriasis development were detected by reverse transcription polymerase chain reaction and western blotting. Treatment with LEU, but not VER and HP extract improved psoriasis-related inflammation via suppression of the PI3K/AKT signaling in IFN-γ/IL-17A/IL-22-stimulated HaCaT cells. Our results suggest that LEU may exhibit therapeutic potential against psoriasis by regulating keratinocyte differentiation through inhibition of the PI3K/AKT pathway.
Highlights
Psoriasis is a chronic, inflammatory, immune-mediated skin pathology, affecting approximately 2–3% of the adult world’s population [1]
We investigated the effect of H. procumbens (HP) extract, munopathogenesis of psoriasis [5,16]
STAT3 together with NF-κB regulates the expression of genes that control cell survival and proliferation, and inhibition of these transcription factors is a promising therapeutic strategy in psoriasis [39]. These results demonstrated that HP extract affected mainly NF-κB-related genes and their activation points towards induction in the immune response and thereby obstructs keratinocytes hyperproliferation
Summary
Inflammatory, immune-mediated skin pathology, affecting approximately 2–3% of the adult world’s population [1]. It is manifested mainly with psoriatic lesions and is associated with serious complications such as psoriatic arthritis, obesity, sleep apnea, depression and certain autoimmune diseases [1,2,3,4]. Chronic psoriasis is characterized with a deterioration in the quality of life. The pathophysiology of psoriasis is characterized by hyperproliferation, dysfunctional apoptosis and abnormal differentiation of keratinocytes that are accompanied with infiltration of immune cells in the dermis and epidermis [1,5,6]. The percentage of proliferative cell populations are found to be increased in the basal and suprabasal layers in psoriasis
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