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白细胞介素-10(IL-10)治疗与克罗恩病肠道纤维化小鼠模型中抑制素的表达有关。

IL-10 treatment is associated with prohibitin expression in the Crohn's disease intestinal fibrosis mouse model.

机构信息

Department of Gastroenterology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, China.

出版信息

Mediators Inflamm. 2013;2013:617145. doi: 10.1155/2013/617145. Epub 2013 Apr 14.

DOI:10.1155/2013/617145
PMID:23690666
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3649775/
Abstract

Prohibitin, which can inhibit oxidative stress and mitochondrial dysfunction, has been shown to have significant anti-inflammatory activities. Here, we investigate the effects of altering prohibitin levels in affected tissues in the interleukin-10 knockout (IL-10KO) mouse model with intestinal fibrosis. The aim of this study is to investigate the effects of IL-10 on prohibitin and the role of prohibitin in intestinal fibrosis of murine colitis. After the mice were treated with IL-10, prohibitin expression and localization were evaluated in IL-10KO and wild-type (WT, 129/SvEv) mice. The colon tissue was then investigated and the potential pathogenic molecular mechanisms were further studied. Fluorescence-based quantitative polymerase chain reaction (FQ-PCR) and immunohistochemistry assays revealed a significant upregulation of prohibitin with IL-10 treatment. Furthermore, IL-10 decreases inflammatory cytokines and TGF-β1 in the IL-10KO model of Crohn's disease and demonstrates a promising trend in decreasing tissue fibrosis. In conclusion, we hypothesize that IL-10 treatment is associated with increased prohibitin and would decrease inflammation and fibrosis in an animal model of Crohn's disease. Interestingly, prohibitin may be a potential target for intestinal fibrosis associated with inflammatory bowel disease (IBD).

摘要

抑制素可以抑制氧化应激和线粒体功能障碍,具有显著的抗炎活性。在这里,我们研究了改变白细胞介素 10 敲除(IL-10KO)小鼠模型中受影响组织中抑制素水平对肠道纤维化的影响。本研究旨在研究白细胞介素 10 对抑制素的影响以及抑制素在鼠结肠炎肠道纤维化中的作用。在对小鼠进行白细胞介素 10 处理后,评估了白细胞介素 10KO 和野生型(WT,129/SvEv)小鼠中抑制素的表达和定位。然后研究了结肠组织,并进一步研究了潜在的致病分子机制。荧光定量聚合酶链反应(FQ-PCR)和免疫组织化学检测显示,白细胞介素 10 处理后抑制素显著上调。此外,白细胞介素 10 降低了克罗恩病 IL-10KO 模型中的炎症细胞因子和 TGF-β1,并显示出在降低组织纤维化方面有良好的趋势。总之,我们假设白细胞介素 10 治疗与抑制素的增加有关,并可在克罗恩病的动物模型中减轻炎症和纤维化。有趣的是,抑制素可能是与炎症性肠病(IBD)相关的肠道纤维化的一个潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/002e66913f2c/MI2013-617145.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/a5064537265e/MI2013-617145.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/da7cd4bc302b/MI2013-617145.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/77f8982d7655/MI2013-617145.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/10b83e5cc832/MI2013-617145.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/002e66913f2c/MI2013-617145.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/a5064537265e/MI2013-617145.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/da7cd4bc302b/MI2013-617145.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/77f8982d7655/MI2013-617145.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/10b83e5cc832/MI2013-617145.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7cd/3649775/002e66913f2c/MI2013-617145.005.jpg

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Resistance to bleomycin-induced lung fibrosis in MMP-8 deficient mice is mediated by interleukin-10.
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Intestinal Fibrosis in Inflammatory Bowel Disease and the Prospects of Mesenchymal Stem Cell Therapy.炎症性肠病中的肠纤维化和间充质干细胞治疗的前景。
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