Dan-Zhi-Yin formula against IL-17A/F-induced chemokines via JNK pathway in mouse embryo fibroblasts NIH 3T3 cells

被引:0
作者
Xu, Lin [1 ]
Zhuang, Yulong [1 ]
Huang, Wenling [2 ]
Gong, Xin [2 ]
Jin, Zhe [2 ]
机构
[1] Beijing Univ Tradit Chinese Med, Beijing, Peoples R China
[2] Beijing Univ Tradit Chinese Med, Dept Gynecol, Dongfang Hosp, 6 Fangxingyuan 1 Qu, Beijing 100078, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2017年 / 10卷 / 09期
基金
中国国家自然科学基金;
关键词
IL-17A/F; DZY; JNK; IL-17RA; IL-17RC; mouse embryo fibroblasts; INTERLEUKIN-17; FAMILY; TNF-ALPHA; IN-VITRO; IL-17; EXPRESSION; CYTOKINE; INHIBITION; ACTIVATION; KINASE; CELLS;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Dan-Zhi-Yin formula (DZY) is a traditional Chinese medicine formula consisting of 8 herbs, which has been used to treat chronic pelvic inflammation and pelvic pain. The aim of the present study was to observe the mechanism of DZY on IL-17A/F-induced chemokines in the mouse embryonic fibroblasts (NIH 3T3). The viability of cells was determined by MTT assay. We evaluated the expression of the chemokines monocyte chemoattractant protein- 1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) by ELISA and real-time RT-PCR. The phosphorylation of JNK was assessed by Cytometric Bead Array. IL-17RA and IL-17RC were inhibited by small interfering RNA (siRNA). Our study demonstrated that IL-17A/F were able to increase the gene levels and protein secretion of MCP-1 and MIP-2. However, the DZY could disrupt the expression of MCP-1 and MIP-2 stimulated by IL-17A/F. We observed that IL-17A/F could induce JNK activation and that pharmacological inhibitors of JNK (SP600125) blocked the IL-17A/F mediated MCP-1 and MIP-2 release. DZY could inhibited JNK expression at each time point, compared with Il-17A/F stimulated group alone. In addition, we also found that NIH 3T3 cells expressed IL-17 receptors. The expression of MCP-1 and MIP-2 stimulated by IL-17A/F could be reduced by inhibiting IL-17RA or IL-17RC expression via siRNA. In conclusion, IL-17A/F could induce the expression of MCP-1 and MIP-2 through JNK pathway in NIH 3T3 cells. However, DZY can inhibit IL-17A/F-induce MCP-1 and MIP-2 expression which might be regulated by JNK pathway. All these above indicate that DZY plays a role in anti-inflammatory process in NIH 3T3 cells.
引用
收藏
页码:13123 / 13132
页数:10
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