期刊:Current traditional medicine [Bentham Science] 日期:2024-10-23卷期号:11
标识
DOI:10.2174/0122150838312001241002094020
摘要
aims: To study investigates the mechanism of action of Yinxieling in the treatment of psoriasis. background: Psoriasis is a chronic skin disease characterized by erythema, scaling, and thickening. Yinxieling is a representative prescription for treating psoriasis developed by Professor Guowei Xuan, a master of traditional Chinese medicine. Keratin 17 is a key biomarker for the diagnosis and treatment of psoriasis, and its overexpression has been shown to impair mitochondrial function. objective: To study investigates the mechanism of action of Yinxieling in the treatment of psoriasis. method: In vivo, BALB/c mice were induced by imiquimod to create psoriasis-like mice model. Different doses of Yinxieling were administered to the psoriasis-like mice and PASI scores, thickness of epidermis and Keratin 17 expression of psoriasis-like mice were measured. In vitro, HaCaT cells were induced by IL-17A, IL-22 and TNF-alpha to establish psoriasis-like cells model. Yinxieling with different concentrations were administered to the psoriasis-like cells and Keratin 17 expression, adenosine triphosphate levels and oxygen consumption rates were measured. Furthermore, the psoriasis-like cells were transfected with keratin 17 plasmids. Yinxieling intervened in these psoriasis-like cells with continuous high expression of keratin 17 and adenosine triphosphate levels and oxygen consumption rates were measured. result: Yinxieling significantly improved PASI scores and decreased their epidermal thickness in psoriasis-like mice; Yinxieling also inhibited Krt17 expression in psoriasis-like mice and cells. Yinxieling improved ATP levels and oxygen consumption rate in psoriasis-like cells, and this effect of Yinxieling was abolished when the psoriasis-like cells were transfected with keratin 17 plasmids. conclusion: Yinxieling inhibits keratin 17 to enhance mitochondrial function and ameliorates psoriasis-like lesions. other: None