Abstract
A cream formulation containing Artemisia capillaris (AC) extract (ACE) was developed for psoriasis therapy. Although ACE can be dissolved in organic solvents, its topical application is restricted because of toxicities. Therefore, a cream formulation was developed for the convenient and safe local application of ACE on skin lesions. The antipsoriatic properties of the ACE cream were evaluated using an imiquimod- (IMQ-) induced psoriasis-like mouse model. In psoriasis-like mouse models, the cumulative score (redness, thickness, and scaling) of the IMQ + ACE cream group was significantly lower than those of the other groups on day 4 (p < 0.05). The results of the hematoxylin and eosin staining of skin tissues revealed that the epidermal thickness value of the IMQ + ACE cream group was significantly lower than those of the other experimental groups (p < 0.05). The expression level of intracellular adhesion molecule-1 (ICAM-1), which indicates the leukocyte infiltration into the skin and subsequent interactions with keratinocytes, was also lower in the IMQ + ACE cream group than in the IMQ group. These results indicate that ACE cream formulation could be used safely and conveniently for psoriasis treatment.
Highlights
Psoriasis is an autoimmune disease characterized by itchy, red, and scaly skin patches [1]
All solvents were of high-performance liquid chromatography (HPLC) grade and the other chemicals were of analytical grade
Because of the presence of pharmaceutical excipients in the cream formulation, the amounts of the four markers slightly differed from those values previously reported in ACE [8]
Summary
Psoriasis is an autoimmune disease characterized by itchy, red, and scaly skin patches [1]. The pathogenesis of psoriasis involves the abnormally rapid growth of the skin epidermis. The transfer of immune cells (i.e., dendritic, macrophage, and T cells) from the dermis to the epidermis and secretion of cytokines (i.e., interleukin[IL-] 1β, IL-6, and IL-22 and tumor necrosis factor- [TNF] α) may stimulate the proliferation of keratinocytes [3]. DNA, which can be released from dying cells, may act as an inflammatory stimulus in psoriatic lesion and could lead to the secretion of cytokines (i.e., IL-1, IL-6, and TNF-α) from keratinocytes [3]. The increase of dendritic cells in psoriatic lesions and its involvement in the proliferation of T cells and type 1 helper T cells may be one of mechanisms of psoriasis development [4]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
