Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS)
Accumulating evidence has revealed the anti-inflammatory effects of arbutin against various diseases. However, the effects of arbutin are not clarified in ulcerative colitis. This study was intended to investigate the protective effects and mechanisms of arbutin on DSS-induced colitis. Hematoxylin e...
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oai:doaj.org-article:e144612cfff54c6e8fcdbddb61f254452021-11-17T14:21:59ZArbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS)2165-59792165-598710.1080/21655979.2021.2005746https://doaj.org/article/e144612cfff54c6e8fcdbddb61f254452021-11-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2005746https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Accumulating evidence has revealed the anti-inflammatory effects of arbutin against various diseases. However, the effects of arbutin are not clarified in ulcerative colitis. This study was intended to investigate the protective effects and mechanisms of arbutin on DSS-induced colitis. Hematoxylin eosin staining was performed to determine the pathological damage of intestinal tissue in mice. Inflammatory factors levels in intestinal tissue were detected by enzyme linked immunosorbent assay (ELISA) assay. TUNEL staining showed the apoptosis levels of cells. Intestinal permeability was analyzed using the application of Fluorescein isothiocyanate Dextran (FD) 4. The levels of Zona Occludens 1 (ZO-1), occluding and claudin-1, and the related proteins in MAPK/ELK1 pathway were analyzed by Western blot. DSS promotes pathological injury, the levels of pro-inflammatory factors containing tumor necrosis factor alpha (TNF-α), Interleukin- 6 (IL-6) and myeloperoxidase (MPO), and cell apoptosis in the mouse colon. Additionally, intestinal permeability was increased and the levels of tight function-related proteins were increased following DSS induction. Its effects could be greatly improved by arbutin. Arbutin exerted effects by eliciting anti-inflammatory effects and maintaining normal intestinal mucosal barrier function, the action mechanism of which could be associated with MAPK/ELK1 pathway.Chuan ZhangHuiping ZhuHui JieHengyue DingHongwen SunTaylor & Francis Grouparticlearbutinulcerative colitisinflammationapoptosisjnkp38BiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021) |
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arbutin ulcerative colitis inflammation apoptosis jnk p38 Biotechnology TP248.13-248.65 |
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arbutin ulcerative colitis inflammation apoptosis jnk p38 Biotechnology TP248.13-248.65 Chuan Zhang Huiping Zhu Hui Jie Hengyue Ding Hongwen Sun Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
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Accumulating evidence has revealed the anti-inflammatory effects of arbutin against various diseases. However, the effects of arbutin are not clarified in ulcerative colitis. This study was intended to investigate the protective effects and mechanisms of arbutin on DSS-induced colitis. Hematoxylin eosin staining was performed to determine the pathological damage of intestinal tissue in mice. Inflammatory factors levels in intestinal tissue were detected by enzyme linked immunosorbent assay (ELISA) assay. TUNEL staining showed the apoptosis levels of cells. Intestinal permeability was analyzed using the application of Fluorescein isothiocyanate Dextran (FD) 4. The levels of Zona Occludens 1 (ZO-1), occluding and claudin-1, and the related proteins in MAPK/ELK1 pathway were analyzed by Western blot. DSS promotes pathological injury, the levels of pro-inflammatory factors containing tumor necrosis factor alpha (TNF-α), Interleukin- 6 (IL-6) and myeloperoxidase (MPO), and cell apoptosis in the mouse colon. Additionally, intestinal permeability was increased and the levels of tight function-related proteins were increased following DSS induction. Its effects could be greatly improved by arbutin. Arbutin exerted effects by eliciting anti-inflammatory effects and maintaining normal intestinal mucosal barrier function, the action mechanism of which could be associated with MAPK/ELK1 pathway. |
format |
article |
author |
Chuan Zhang Huiping Zhu Hui Jie Hengyue Ding Hongwen Sun |
author_facet |
Chuan Zhang Huiping Zhu Hui Jie Hengyue Ding Hongwen Sun |
author_sort |
Chuan Zhang |
title |
Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
title_short |
Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
title_full |
Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
title_fullStr |
Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
title_full_unstemmed |
Arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (DSS) |
title_sort |
arbutin ameliorated ulcerative colitis of mice induced by dextran sodium sulfate (dss) |
publisher |
Taylor & Francis Group |
publishDate |
2021 |
url |
https://doaj.org/article/e144612cfff54c6e8fcdbddb61f25445 |
work_keys_str_mv |
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