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

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; surfac...

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Main Authors: Shikui Xu, Aixue Zuo, Zengjun Guo, Chunping Wan
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2017/7416792
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author Shikui Xu
Aixue Zuo
Zengjun Guo
Chunping Wan
author_facet Shikui Xu
Aixue Zuo
Zengjun Guo
Chunping Wan
author_sort Shikui Xu
collection DOAJ
description 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-γ) were detected by flow cytometry. Th1 cell differentiation assay was performed, and mRNA expression in interferon-γ-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-γ and IL-6 secretion, and decreased the proportion of CD11b+Gr-1+ splenic neutrophil. Meanwhile, ECF treatment significantly inhibited the IFN-γ 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-γ-related signaling, including IFN-γ, 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-γ-related signaling.
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institution Kabale University
issn 2314-8861
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publishDate 2017-01-01
publisher Wiley
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series Journal of Immunology Research
spelling doaj-art-92e5fb0ff63f4fef939402bf827d48e92025-02-03T01:04:56ZengWileyJournal of Immunology Research2314-88612314-71562017-01-01201710.1155/2017/74167927416792Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune ResponseShikui Xu0Aixue Zuo1Zengjun Guo2Chunping Wan3School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, ChinaSchool of Pharmacy, Yunnan University of Traditional Chinese Medicine, Kunming 650500, ChinaSchool of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, ChinaCentral Laboratory, The No.1 Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming 650021, ChinaThe 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-γ) were detected by flow cytometry. Th1 cell differentiation assay was performed, and mRNA expression in interferon-γ-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-γ and IL-6 secretion, and decreased the proportion of CD11b+Gr-1+ splenic neutrophil. Meanwhile, ECF treatment significantly inhibited the IFN-γ 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-γ-related signaling, including IFN-γ, 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-γ-related signaling.http://dx.doi.org/10.1155/2017/7416792
spellingShingle Shikui Xu
Aixue Zuo
Zengjun Guo
Chunping Wan
Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
Journal of Immunology Research
title Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
title_full Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
title_fullStr Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
title_full_unstemmed Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
title_short Ethyl Caffeate Ameliorates Collagen-Induced Arthritis by Suppressing Th1 Immune Response
title_sort ethyl caffeate ameliorates collagen induced arthritis by suppressing th1 immune response
url http://dx.doi.org/10.1155/2017/7416792
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AT aixuezuo ethylcaffeateamelioratescollageninducedarthritisbysuppressingth1immuneresponse
AT zengjunguo ethylcaffeateamelioratescollageninducedarthritisbysuppressingth1immuneresponse
AT chunpingwan ethylcaffeateamelioratescollageninducedarthritisbysuppressingth1immuneresponse