Min Ga-Yul, Kim Tae In, Kim Ji-Hye, Cho Won-Kyung, Yang Ju-Hye, Ma Jin-Yeul
Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea.
Chin Med. 2022 Jun 8;17(1):66. doi: 10.1186/s13020-022-00624-5.
Isatis tinctoria L (PLG) is a medicinal herb from the roots of Isatis indigotica Fort (Family Cruciferae). Previous studies have shown that PLG has anti-inflammatory and therapeutic effects against conditions such as acute and chronic hepatitis, various respiratory inflammations, and cancer. The purpose of this study was to define the pharmacological effects of PLG on inflammatory reactions and skin hyperkeratosis, which are the main symptoms of atopic dermatitis (AD), in vivo and in vitro.
For the AD in vivo experiment, 2,4-dinitrochlorobenzene (DNCB) induction and oral administration of PLG were performed on male BALB/c mice for four weeks. For in vitro experiments, keratinocytes were activated using TNF-α/IFN-γ in cultured human keratinocyte (HaCaT) cells. PLG inhibited inflammatory chemokine production and blocked the nuclear translocation of NF-κB p65 in activated keratinocytes.
As a result of oral administration of PLG, dermis and epidermis thickening, as well as eosinophil and mast cell infiltration, were attenuated in AD skin lesions. In addition, the levels of immunoglobulin E (IgE), pro-inflammatory cytokines, and the MAPK/NF-κB signaling pathway were decreased in serum and dorsal skin tissues. Furthermore, PLG inhibited inflammatory chemokine production and blocked the nuclear translocation of NF-κB p65 in activated keratinocytes. In addition, epigoitrin and adenosine, the standard compounds of PLG, were identified as candidate AD compounds.
These results indicate that PLG is a potent therapeutic agent for attenuating symptoms of AD.
菘蓝（PLG）是一种来源于十字花科植物菘蓝（Isatis indigotica Fort）根部的草药。先前的研究表明，PLG对急性和慢性肝炎、各种呼吸道炎症及癌症等病症具有抗炎和治疗作用。本研究的目的是在体内和体外确定PLG对特应性皮炎（AD）的主要症状——炎症反应和皮肤角化过度的药理作用。
在AD体内实验中，对雄性BALB/c小鼠进行2,4-二硝基氯苯（DNCB）诱导并口服PLG，持续四周。在体外实验中，使用肿瘤坏死因子-α/干扰素-γ激活培养的人角质形成细胞（HaCaT）中的角质形成细胞。PLG抑制炎症趋化因子的产生，并阻断活化角质形成细胞中核因子-κB p65的核转位。
口服PLG后，AD皮肤损伤中的真皮和表皮增厚以及嗜酸性粒细胞和肥大细胞浸润减轻。此外，血清和背部皮肤组织中的免疫球蛋白E（IgE）、促炎细胞因子水平以及丝裂原活化蛋白激酶/核因子-κB信号通路均降低。此外，PLG抑制炎症趋化因子的产生，并阻断活化角质形成细胞中核因子-κB p65的核转位。此外，PLG的标准化合物靛玉红和腺苷被鉴定为潜在的AD治疗化合物。
这些结果表明，PLG是一种减轻AD症状的有效治疗剂。
