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Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression
Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protect...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Applied Pharmacology
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430230/ https://www.ncbi.nlm.nih.gov/pubmed/30173501 http://dx.doi.org/10.4062/biomolther.2018.052 |
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author | Wang, Peng-fei Yao, Dan-hua Hu, Yue-yu Li, Yousheng |
author_facet | Wang, Peng-fei Yao, Dan-hua Hu, Yue-yu Li, Yousheng |
author_sort | Wang, Peng-fei |
collection | PubMed |
description | Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile CCl(4) (a mixture of pure CCl(4) and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, 1,25(OH)(2)D(3) (0.5 µg/100 g) and the vehicle were administered simultaneously with CCl(4) to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in CCl(4)-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects. |
format | Online Article Text |
id | pubmed-6430230 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Korean Society of Applied Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-64302302019-03-25 Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression Wang, Peng-fei Yao, Dan-hua Hu, Yue-yu Li, Yousheng Biomol Ther (Seoul) Original Article Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile CCl(4) (a mixture of pure CCl(4) and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, 1,25(OH)(2)D(3) (0.5 µg/100 g) and the vehicle were administered simultaneously with CCl(4) to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in CCl(4)-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects. The Korean Society of Applied Pharmacology 2019-02 2018-09-03 /pmc/articles/PMC6430230/ /pubmed/30173501 http://dx.doi.org/10.4062/biomolther.2018.052 Text en Copyright ©2019, The Korean Society of Applied Pharmacology http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Wang, Peng-fei Yao, Dan-hua Hu, Yue-yu Li, Yousheng Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title | Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title_full | Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title_fullStr | Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title_full_unstemmed | Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title_short | Vitamin D Improves Intestinal Barrier Function in Cirrhosis Rats by Upregulating Heme Oxygenase-1 Expression |
title_sort | vitamin d improves intestinal barrier function in cirrhosis rats by upregulating heme oxygenase-1 expression |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430230/ https://www.ncbi.nlm.nih.gov/pubmed/30173501 http://dx.doi.org/10.4062/biomolther.2018.052 |
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