Cang-ai volatile oil ameliorates imiquimod-induced psoriatic skin lesions by suppressing the ILC3s

伊米奎莫德 哈卡特 银屑病 白细胞介素 免疫学 促炎细胞因子 医学 TLR4型 肿瘤坏死因子α 流式细胞术 药理学 免疫系统 炎症 细胞因子 生物 生物化学 体外
作者
Yuping Lin,Xunqing Yin,Shan Ma,Yongmei Xue,Chunyan Hu,Yuhuan Xie,Yongcheng Zeng,Xiujuan Zhao,Chenghong Du,Yun Sun,Lu Qu,Lei Xiong,Feng Huang
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:326: 117867-117867 被引量:3
标识
DOI:10.1016/j.jep.2024.117867
摘要

Cang-ai volatile oil (CAVO) is an aromatic Chinese medicine with potent antibacterial and immune regulatory properties. While CAVO has been used to treat upper respiratory tract infections, depression, otomycosis, and bacterial infections in the skin, its effect on psoriasis is unknown. This study explores the effect and mechanism of CAVO in psoriasis intervention. The effect of CAVO on the expression of IL-6 and IL-1β was assessed in TNF-α-induced HaCaT cells using enzyme-linked immunosorbent assay (ELISA). Mice were given imiquimod (IMQ) and administered orally with different CAVO doses (0.03 and 0.06 g/kg) for 5 days. The levels of inflammatory cytokines related to group-3 innate lymphoid cells (ILC3s) in the skin were assessed using hematoxylin and eosin (H&E) staining, ELISA, and western blotting (WB). The frequency of ILC3s in mice splenocytes and skin cells was evaluated using flow cytometry. The results demonstrated that CAVO decreased the expression of IL-6 and IL-1β in TNF-α- induced HaCaT cells. CAVO significantly reduced the severity of psoriatic symptoms in IMQ-induced mice. The expression of inflammatory cytokines in the skin, such as IL-1β, IL-6, IL-8, IL-22, IL-23, and IL-17 A were decreased, whereas IL-10 levels were increased. The mRNA expressions of TNF-α, IL-23 A, IL-23 R, IL-22, IL-17 A, and RORγt were down-regulated in skin tissues. CAVO also decreased the levels of NF-κB, STAT3, and JAK2 proteins. CAVO potentially inhibits ILC3s activation to relieve IMQ-induced psoriasis in mice. These effects might be attributed to inhibiting the activation of NF-κB, STAT3, and JAK2 signaling pathways.
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