Yang Ju-Hye, Hwang Youn-Hwan, Gu Min-Jung, Cho Won-Kyung, Ma Jin Yeul
Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea.
Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 701-300, Republic of Korea.
Phytomedicine. 2015 Dec 15;22(14):1262-8. doi: 10.1016/j.phymed.2015.09.006. Epub 2015 Nov 9.
Sanguisorba officinalis L. (SOL) is a perennial plant widely distributed in Asia, its roots are well-known as a traditional herbal medicine to treat burns, chronic intestinal infections, scalds, and inflammation in Korea. Also, the roots of SOL are used for treatment of many types of allergic skin diseases, including urticarial, eczema, and allergic dermatitis.
In this study we investigated the underlying mechanism of anti-inflammatory effect of an ethanol extract of SOL roots (ESOL).
The ability of ESOL to inhibit inflammatory skin disorder was tested in human keratinocyte HaCaT cells.
Viability test using MTT assay were used to determine non-cytotoxic concentrations of ESOL on HaCaT cells. ESOL-mediated inhibition of the tumor necrosis factor (TNF)-α/interferon (IFN)-γ-induced production of pro-inflammatory chemokines-such as macrophage-derived chemokine (MDC), regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-8, and thymus and activation regulated chemokine (TARC)-at the mRNA level was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). The ability of ESOL to reduce the expression of pro-inflammatory marker proteins was evaluated by Western blot analysis and immunocytochemistry.
ESOL reduced the production of MDC, RANTES, IL-8, and TARC in HaCaT cells stimulated with TNF-α/IFN-γ at both protein and mRNA levels. ESOL also suppressed the phosphorylation of signal transducer and activator of transcription (STAT)-1, extracellular signal-regulated kinase (ERK), and inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκB-α) degradation and the nuclear translocation of NF-κB/p65. ESOL exerts anti-inflammatory effects by suppressing the expression of TNF-α/IFN-γ-stimulated chemokines and pro-inflammatory molecules via a blockade NF-κB, STAT-1, and ERK activation.
Our results suggest the preventive potential of ESOL as a herbal medicine for the treatment of inflammatory skin diseases.
地榆是一种多年生植物，广泛分布于亚洲，在韩国，其根部作为治疗烧伤、慢性肠道感染、烫伤和炎症的传统草药而闻名。此外，地榆根还用于治疗多种过敏性皮肤病，包括荨麻疹、湿疹和过敏性皮炎。
在本研究中，我们研究了地榆根乙醇提取物（ESOL）抗炎作用的潜在机制。
在人角质形成细胞HaCaT细胞中测试ESOL抑制炎症性皮肤病的能力。
使用MTT法进行活力测试，以确定ESOL对HaCaT细胞的非细胞毒性浓度。通过实时逆转录-聚合酶链反应（RT-PCR）测定ESOL在mRNA水平上对肿瘤坏死因子（TNF）-α/干扰素（IFN）-γ诱导的促炎趋化因子（如巨噬细胞衍生趋化因子（MDC）、活化调节正常T细胞表达和分泌因子（RANTES）、白细胞介素（IL）-8和胸腺激活调节趋化因子（TARC））产生的抑制作用。通过蛋白质印迹分析和免疫细胞化学评估ESOL降低促炎标记蛋白表达的能力。
ESOL在蛋白质和mRNA水平上均降低了TNF-α/IFN-γ刺激的HaCaT细胞中MDC、RANTES、IL-8和TARC的产生。ESOL还抑制了信号转导和转录激活因子（STAT）-1、细胞外信号调节激酶（ERK）的磷酸化，并抑制了B细胞中κ轻链多肽基因增强子的核因子抑制剂α（IκB-α）的降解以及NF-κB/p65的核转位。ESOL通过阻断NF-κB、STAT-1和ERK激活来抑制TNF-α/IFN-γ刺激的趋化因子和促炎分子的表达，从而发挥抗炎作用。
我们的结果表明ESOL作为治疗炎症性皮肤病的草药具有预防潜力。
