IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model
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 fibro...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/617145 |
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| _version_ | 1849685108355760128 |
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| author | C. Yuan W.-X. Chen J.-S. Zhu N.-W. Chen Y.-M. Lu Y.-X. Ou H.-Q. Chen |
| author_facet | C. Yuan W.-X. Chen J.-S. Zhu N.-W. Chen Y.-M. Lu Y.-X. Ou H.-Q. Chen |
| author_sort | C. Yuan |
| collection | DOAJ |
| description | 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). |
| format | Article |
| id | doaj-art-c250f0e82a7b4bdb89e7fae218697704 |
| institution | DOAJ |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c250f0e82a7b4bdb89e7fae2186977042025-08-20T03:23:15ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/617145617145IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse ModelC. Yuan0W.-X. Chen1J.-S. Zhu2N.-W. Chen3Y.-M. Lu4Y.-X. Ou5H.-Q. Chen6Department of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaDepartment of General Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, ChinaProhibitin, 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).http://dx.doi.org/10.1155/2013/617145 |
| spellingShingle | C. Yuan W.-X. Chen J.-S. Zhu N.-W. Chen Y.-M. Lu Y.-X. Ou H.-Q. Chen IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model Mediators of Inflammation |
| title | IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model |
| title_full | IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model |
| title_fullStr | IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model |
| title_full_unstemmed | IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model |
| title_short | IL-10 Treatment Is Associated with Prohibitin Expression in the Crohn’s Disease Intestinal Fibrosis Mouse Model |
| title_sort | il 10 treatment is associated with prohibitin expression in the crohn s disease intestinal fibrosis mouse model |
| url | http://dx.doi.org/10.1155/2013/617145 |
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