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Gene. 2012 Oct 25;508(2):157-64. doi: 10.1016/j.gene.2012.07.045. Epub 2012 Aug 8.
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The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings.IL-17 在银屑病发病机制中的新作用：临床前和临床研究发现。
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J Dermatol Sci. 2012 Feb;65(2):134-40. doi: 10.1016/j.jdermsci.2011.11.011. Epub 2011 Dec 8.
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Cluvenone induces apoptosis via a direct target in mitochondria: a possible mechanism to circumvent chemo-resistance?氯维酮通过线粒体的直接靶标诱导细胞凋亡：规避化疗耐药性的一种可能机制？
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IL-17A upregulates keratin 17 expression in keratinocytes through STAT1- and STAT3-dependent mechanisms.白细胞介素-17A 通过 STAT1 和 STAT3 依赖的机制上调角质形成细胞中角蛋白 17 的表达。
J Invest Dermatol. 2011 Dec;131(12):2401-8. doi: 10.1038/jid.2011.222. Epub 2011 Jul 28.
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Mitochondria as targets for cancer therapy.线粒体作为癌症治疗的靶点。
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Shikonin, acetylshikonin, and isobutyroylshikonin inhibit VEGF-induced angiogenesis and suppress tumor growth in lewis lung carcinoma-bearing mice.紫草素、乙酰紫草素和异丁酰紫草素可抑制血管内皮生长因子（VEGF）诱导的血管生成，并抑制荷Lewis肺癌小鼠的肿瘤生长。
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紫草素通过干扰信号转导和转录激活因子3（STAT3）信号通路，抑制干扰素-γ（IFN-γ）诱导的人永生化角质形成细胞（HaCaT细胞）中角蛋白17（K17）的过表达。

Shikonin inhibits IFN-γ-induced K17 over-expression of HaCaT cells by interfering with STAT3 signaling.

作者信息

Liu Lili, Wu Yan, Cao Kai, Xu Yuan-Yuan, Gao Xing-Hua, Chen Hong-Duo, Geng Long

机构信息

Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China ; Department of Dermatology, Hospital of Beihua University Jilin, China.

Department of Dermatology, First Hospital of China Medical University Shenyang 110001, Liaoning, China.

出版信息

Int J Clin Exp Pathol. 2015 Aug 1;8(8):9202-7. eCollection 2015.

PMID:26464667
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4583899/
Abstract

OBJECTIVES

We hypothesized that interferon-γ (IFN-γ) induces K17 over-expression in HaCaT cells by activating STAT3 and that Sh might inhibit the over-expression through interference of STAT3 signaling.

METHODS

In vitro culture of HaCaT cells treated with IFN-γ and measurement of K17 protein by enzyme linked immunosorbent assay.

RESULTS

The level of K17 protein (one kind of keratin protein) in the supernatant induced by IFN-γ was significantly reduced by Shikonin at various concentrations. Interference of STAT3 suppressed the effect of IFN-γ on K17 expression at both mRNA and protein levels. The over-expression of K17 in IFN-γ-induced HaCaT cells was significantly suppressed by 2 µg/L Shikonin. Interfering with STAT3 signaling with 2 µg/L Shikonin resulted in an intermediate level of IFN-γ-induced K17 protein in HaCaT cells.

CONCLUSIONS

These data demonstrate that IFN-γ induces K17 protein over-expression of HaCaT cells by activating STAT3 and Shikonin may inhibit the over-expression partly through interference of STAT3.

摘要

目的

我们推测干扰素-γ（IFN-γ）通过激活信号转导和转录激活因子3（STAT3）诱导人永生化角质形成细胞（HaCaT细胞）中角蛋白17（K17）的过表达，而紫草素（Sh）可能通过干扰STAT3信号传导来抑制这种过表达。

方法

对用IFN-γ处理的HaCaT细胞进行体外培养，并用酶联免疫吸附测定法测量K17蛋白。

结果

不同浓度的紫草素均可显著降低IFN-γ诱导的上清液中K17蛋白（一种角蛋白）的水平。干扰STAT3在mRNA和蛋白质水平均抑制了IFN-γ对K17表达的影响。2μg/L的紫草素可显著抑制IFN-γ诱导的HaCaT细胞中K17的过表达。用2μg/L紫草素干扰STAT3信号传导导致HaCaT细胞中IFN-γ诱导的K17蛋白处于中等水平。

结论

这些数据表明，IFN-γ通过激活STAT3诱导HaCaT细胞中K17蛋白的过表达，而紫草素可能部分通过干扰STAT3来抑制这种过表达。