软枣猕猴桃水溶性提取物。前Miq。紫苏(perula frutescens,L.)Britton,ACTPER,通过激活HaCaT细胞中的AhR信号,改善小鼠皮肤干燥诱导的瘙痒,并促进丝聚糖蛋白的表达。

PubMed ID
G H
发表日期 2019年Jun月

原始出处 营养物
Nutrients
作者 Lee  Wonwoo  Jeong  Yoonseon  Park  Jong-Hyung  Lee  Chang Hyung  Yun  Nayoung  Lee  Doo Suk  Nam  In-Jeong  Kim  Jung-Dong  Yoon  Kee Dong  Son  Miwon  Kim  Sunyoung 

文献标题 软枣猕猴桃水溶性提取物。前Miq。紫苏(perula frutescens,L.)Britton,ACTPER,通过激活HaCaT细胞中的AhR信号,改善小鼠皮肤干燥诱导的瘙痒,并促进丝聚糖蛋白的表达。
Water-Soluble Extract from Actinidia arguta (Siebold & Zucc.) Planch. ex Miq. and Perilla frutescens (L.) Britton, ACTPER, Ameliorates a Dry Skin-Induced Itch in a Mice Model and Promotes Filaggrin Expression by Activating the AhR Signaling in HaCaT Cells.
Water-Soluble Extract from Actinidia arguta (Siebold & Zucc.) Planch. ex Miq. and Perilla frutescens (L.) Britton, ACTPER, Ameliorates a Dry Skin-Induced Itch in a Mice Model and Promotes Filaggrin Expression by Activating the AhR Signaling in HaCaT Cells.

文献摘要

瘙痒是许多皮肤病的主要症状,病因复杂,涉及多种因素。例如,目前的治疗方法对于解决干性皮肤引起的瘙痒是无效的。我们开发了一种植物提取物ACTPER,它是由软枣猕猴桃和紫苏的混合物制成的,传统上用于治疗瘙痒。在我们的实验中,ACTPER作为研究药物的质量通过基于细胞的生物测定以及使用两种化学标记的高效液相色谱(HPLC)来控制。在丙酮诱导的小鼠皮肤干燥模型中,口服ACTPER可减轻与皮肤干燥相关的皮肤特性和瘙痒行为。通过定量逆转录聚合酶链反应(RT-PCR)和免疫荧光分析,参与调节皮肤屏障功能的关键因子丝状聚集蛋白(filagrin)基因的RNA和蛋白质表达显著增加。为了在分子水平上理解潜在的机制,用不同浓度的ACTPER处理人角质形成细胞系HaCaT细胞。我们发现ACTPER确实以剂量依赖的方式上调了丝聚糖蛋白的蛋白表达。来自包含外源反应元件(XRE)的报告质粒和芳香烃受体(AhR)的化学拮抗剂的实验数据表明,ACTPER介导的丝聚糖蛋白的上调是通过激活AhR信号通路来控制的。分子对接模拟研究预测ACTPER可能含有直接与AhR结合的化合物。综上所述,我们的研究结果表明ACTPER可能提供了一个平台,在此基础上可以开发出多种安全有效的治疗瘙痒的药物。


With a complex etiology involving multiple factors, the condition known as itch is a primary symptom of many skin diseases. Current treatment methods are ineffective for addressing itches caused by dry skin, for example. We developed a botanical extract, ACTPER, made from a mixture of Actinidia arguta and Perilla frutescens, which have traditionally been used to treat itch. The quality of ACTPER as a research agent was controlled in our experiment by cell-based bioassays, as well as by high-performance liquid chromatography (HPLC), using two chemical markers. In the acetone-induced dry skin mice model, the oral administration of ACTPER alleviated dry skin-related skin properties and itching behavior. The RNA and protein expression of the filament aggregating protein (filaggrin) gene, a key factor involved in the regulation of skin barrier function, was significantly increased, as measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence assay. To understand the underlying mechanism(s) at the molecular level, HaCaT cells, a human keratinocyte-derived cell line, were treated with various concentrations of ACTPER. We found that the protein expression of filaggrin was indeed upregulated by ACTPER in a dose dependent manner. Data from experiments involving the reporter plasmid containing the xenobiotic response element (XRE), and the chemical antagonist for the aryl hydrocarbon receptor (AhR), indicated that the ACTPER-mediated upregulation of filaggrin was controlled through the activation of the AhR signaling pathway. The molecular docking simulation study predicted that ACTPER might contain chemical compounds that bind directly to AhR. Taken together, our results suggest that ACTPER may provide the platform, based upon which a variety of safe and effective therapeutic agents can be developed to treat itch.

With a complex etiology involving multiple factors, the condition known as itch is a primary symptom of many skin diseases. Current treatment methods are ineffective for addressing itches caused by dry skin, for example. We developed a botanical extract, ACTPER, made from a mixture of Actinidia arguta and Perilla frutescens, which have traditionally been used to treat itch. The quality of ACTPER as a research agent was controlled in our experiment by cell-based bioassays, as well as by high-performance liquid chromatography (HPLC), using two chemical markers. In the acetone-induced dry skin mice model, the oral administration of ACTPER alleviated dry skin-related skin properties and itching behavior. The RNA and protein expression of the filament aggregating protein (filaggrin) gene, a key factor involved in the regulation of skin barrier function, was significantly increased, as measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence assay. To understand the underlying mechanism(s) at the molecular level, HaCaT cells, a human keratinocyte-derived cell line, were treated with various concentrations of ACTPER. We found that the protein expression of filaggrin was indeed upregulated by ACTPER in a dose dependent manner. Data from experiments involving the reporter plasmid containing the xenobiotic response element (XRE), and the chemical antagonist for the aryl hydrocarbon receptor (AhR), indicated that the ACTPER-mediated upregulation of filaggrin was controlled through the activation of the AhR signaling pathway. The molecular docking simulation study predicted that ACTPER might contain chemical compounds that bind directly to AhR. Taken together, our results suggest that ACTPER may provide the platform, based upon which a variety of safe and effective therapeutic agents can be developed to treat itch.


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