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佩兰抑制特应性皮炎样皮肤损伤。

Salvia plebeia suppresses atopic dermatitis-like skin lesions.

机构信息

BK21 Plus KNU Biomedical Convergence Program, Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea.

出版信息

Am J Chin Med. 2014;42(4):967-85. doi: 10.1142/S0192415X1450061X.

DOI:10.1142/S0192415X1450061X
PMID:25004886
Abstract

Salvia plebeia R. Br. (Lamiaceae) has been used for folk medicines in Asian countries, including Korea and China, to treat skin inflammatory diseases and asthma. In this study, we investigated the effects of S. plebeia extract (SPE) on atopic dermatitis (AD)-like skin lesions and defined underlying mechanisms of action. We established an AD model in BALB/c mice by repeated local exposure of house dust mite extract (Dermatophagoides farinae extract, DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. The oral administration of SPE decreased AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. SPE suppressed mast cell infiltration into the ear and serum histamine level. SPE inhibited Th1/Th2/Th17 phenotype CD4(+) T lymphocytes expansion in the lymph node and the expression of Th1/Th2/Th17 cytokines in the ear tissue. To define the underlying mechanisms of action, the tumor necrosis factor (TNF)-α and interferon (IFN)-γ activated human keratinocytes (HaCaT) model was used. SPE significantly suppressed the expression of cytokines and chemokines through the down-regulation of mitogen-activated protein kinases, nuclear factor-κB, and STAT1 in HaCaT cells. Taken together, our results suggest that SPE might be a candidate for the treatment of AD.

摘要

野兰香(唇形科)已被亚洲国家(包括韩国和中国)用于民间药物,以治疗皮肤炎症性疾病和哮喘。在这项研究中,我们研究了野兰香提取物(SPE)对特应性皮炎(AD)样皮肤损伤的影响,并确定了其作用机制。我们通过反复局部暴露于屋尘螨提取物(粉尘螨提取物,DFE)和 2,4-二硝基氯苯(DNCB)到耳朵,建立了 BALB/c 小鼠 AD 模型。反复替代 DFE/DNCB 处理导致 AD 样皮肤损伤。SPE 的口服给药基于耳朵厚度和组织病理学分析,降低了 AD 症状,同时降低了血清 IgE 和 IgG2a 水平。SPE 抑制了肥大细胞浸润到耳朵和血清组织胺水平。SPE 抑制了淋巴结中 CD4(+)T 淋巴细胞 Th1/Th2/Th17 表型的扩张,以及耳组织中 Th1/Th2/Th17 细胞因子的表达。为了定义作用机制,使用肿瘤坏死因子(TNF)-α和干扰素(IFN)-γ激活的人角质形成细胞(HaCaT)模型。SPE 通过下调 HaCaT 细胞中的丝裂原活化蛋白激酶、核因子-κB 和 STAT1,显著抑制了细胞因子和趋化因子的表达。总之,我们的结果表明 SPE 可能是治疗 AD 的候选药物。

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