Ameliorative effects of total coumarins from the fructus of Cnidium monnieri (L.) Cuss. on 2, 4‐dinitrochlorobenzene‐induced atopic dermatitis in rats. (26th February 2021)

• Record Type: Journal Article
• Authors: Yu, Zhijie; Deng, Ting; Wang, Ping; Sun, Tao; Xu, Ying
• Is Part Of: Phytotherapy research. Volume 35:Number 6(2021)
• Page Start: 3310
• Page End: 3324
• Publication Date: 2021-02-26
• Subjects: atopic dermatitis -- Cnidium monnieri -- immune response -- MAPKs pathway -- skin barrier function -- topical use; Materia medica, Vegetable -- Periodicals; Botany, Medical -- Periodicals; Medicinal plants -- Periodicals; Plant Extracts -- therapeutic use -- Periodicals; Plants, Medicinal -- Periodicals; 581.634
• DOI: 10.1002/ptr.7052
• Languages: English
• ISSNs: 0951-418X

Abstract

Abstract : Atopic dermatitis (AD), which is characterized by intense pruritus and serious inflammation, is a chronic skin disease. Modern studies have testified that the total coumarins from the fructus of Cnidium monnieri (TCFC) possess evident biological activities based on their coumarin compounds. The purpose of this manuscript is to investigate the effects of topical use of TCFC on immune response, inflammation, and skin barrier function in rats with 2, 4‐dinitrochlorobenzene (DNCB)‐induced AD. Results indicated that the skin lesion scores of rats were obviously reduced after the management of TCFC, and the spleen and thymus indices also were markedly repressed. TCFC significantly inhibited the overproduction of TNF‐α, interferon‐γ, interleukin (IL)‐4, IL‐13, thymic stromal lymphopoietin, and immunoglobulin E; the epidermal thickness and number of mast cells were notably decreased. The western blot experiment was conducted to determine the effects of TCFC on the mitogen‐activated protein kinases signaling pathway. Results indicated that phosphorylation of extracellular signal‐regulated kinases, p38, and c‐Jun amino‐terminal kinases was significantly blocked by TCFC. In addition, TCFC could upregulate the expression of filaggrin in dorsal skin, which means that TCFC showed a protective effect on skin barrier disruption. Furthermore, TCFC downregulated the levels of IL‐1β, IL‐4, IL‐31, and TSLP mRNA and upregulated the expression of filaggrin mRNA in the dorsal skin of rats. Our research demonstrated the ameliorative effects of TCFC on AD‐like rats by inhibiting immune response and inflammation and recovering skin barrier function.