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Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response

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机构: [1]School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, China. [2]Yunnan Institute for Food and Drug Control, Kunming 650011, China. [3]School of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming 650500, China. [4]Central Laboratory, The No.1 Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming 650021, China.
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The present study was designed to assess the antiarthritic potential of ECF in collagen-induced arthritis (CIA) and explore its underlying mechanism. Methods. In vitro, lymphocyte proliferation assay was measured by CCK-8 kit. In vivo, the therapeutic potential of ECF on CIA was investigated; surface marker, Treg cell, and intracellular cytokines (IL-17A and IFN-��) were detected by flow cytometry. Th1 cell differentiation assay was performed, and mRNA expression in interferon-��-related signaling was examined by q-PCR analysis. Results. In vitro, ECF markedly inhibited the proliferation of splenocytes in response to ConA and anti-CD3. In vivo, ECF treatment reduced the severity of CIA, inhibited IFN-�� and IL-6 secretion, and decreased the proportion of CD11b+Gr-1+ splenic neutrophil. Meanwhile, ECF treatment significantly inhibited the IFN-�� expression in CD4+T cell without obviously influencing the development of Th17 cells and T regulatory cells. In vitro, ECF suppressed the differentiation of naive CD4+ T cells into Th1. Furthermore, ECF intensely blocked the transcriptional expression in interferon-��-related signaling, including IFN-��, T-bet, STAT1, and STAT4. Conclusion. Our results indicated that ECF exerted antiarthritic potential in collagen-induced arthritis by suppressing Th1 immune response and interferon-��-related signaling.

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出版当年[2017]版:
大类 | 3 区 医学
小类 | 3 区 免疫学
最新[2023]版:
大类 | 3 区 医学
小类 | 4 区 免疫学
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第一作者机构: [1]School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, China. [2]Yunnan Institute for Food and Drug Control, Kunming 650011, China.
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