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The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion
BACKGROUND/AIM: Even though interleukin-1 receptor antagonist, IL-1Ra, is used in certain inflammatory diseases, its effect on ischemia-reperfusion injury is a current research topic. We aimed to investigate the protective effects of anakinra, an IL-1Ra, on the I/R induced intestinal injury. MATERI...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Scientific and Technological Research Council of Turkey
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8569752/ https://www.ncbi.nlm.nih.gov/pubmed/33843175 http://dx.doi.org/10.3906/sag-2008-258 |
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author | KANDEMİR, Muhammed YAŞAR, Necdet Fatih ÖZKURT, Mete ÖZYURT, Rumeysa BEKTUR AYKANAT, Nuriye Ezgi ERKASAP, Nilüfer |
author_facet | KANDEMİR, Muhammed YAŞAR, Necdet Fatih ÖZKURT, Mete ÖZYURT, Rumeysa BEKTUR AYKANAT, Nuriye Ezgi ERKASAP, Nilüfer |
author_sort | KANDEMİR, Muhammed |
collection | PubMed |
description | BACKGROUND/AIM: Even though interleukin-1 receptor antagonist, IL-1Ra, is used in certain inflammatory diseases, its effect on ischemia-reperfusion injury is a current research topic. We aimed to investigate the protective effects of anakinra, an IL-1Ra, on the I/R induced intestinal injury. MATERIALS AND METHODS: The rat model of intestinal ischemia-reperfusion was induced. Rats were randomized into 4 groups: (group 1) control group, (group 2) I/R group, (group 3 and 4) treatment groups (50 mg/kg and 100 mg/kg, respectively). Gene expressions of caspase-3, TNF-α, IL-1α, IL-6, and apoptotic cells in tissue samples were evaluated by PCR and TUNEL methods, respectively. Plasma levels of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were studied by the ELISA method and tissue samples were examined histopathologically as well. RESULTS: Anakinra inhibited the expression of IL-1α, IL-6, and TNF-α and decreased the SOD, CAT, and MDA caused by ischemia-reperfusion injury in both treatment groups. Caspase-3 expression and TUNEL-positive cell number in treatment groups were also less. Histopathologically, anakinra better preserved the villous structure of the small intestine at a dose of 100 mg/kg than 50 mg/kg. CONCLUSION: Anakinra decreased the intestinal damage caused by ischemia-reperfusion and a dose of 100 mg/kg was found to be histopathologically more effective. |
format | Online Article Text |
id | pubmed-8569752 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Scientific and Technological Research Council of Turkey |
record_format | MEDLINE/PubMed |
spelling | pubmed-85697522021-11-17 The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion KANDEMİR, Muhammed YAŞAR, Necdet Fatih ÖZKURT, Mete ÖZYURT, Rumeysa BEKTUR AYKANAT, Nuriye Ezgi ERKASAP, Nilüfer Turk J Med Sci Article BACKGROUND/AIM: Even though interleukin-1 receptor antagonist, IL-1Ra, is used in certain inflammatory diseases, its effect on ischemia-reperfusion injury is a current research topic. We aimed to investigate the protective effects of anakinra, an IL-1Ra, on the I/R induced intestinal injury. MATERIALS AND METHODS: The rat model of intestinal ischemia-reperfusion was induced. Rats were randomized into 4 groups: (group 1) control group, (group 2) I/R group, (group 3 and 4) treatment groups (50 mg/kg and 100 mg/kg, respectively). Gene expressions of caspase-3, TNF-α, IL-1α, IL-6, and apoptotic cells in tissue samples were evaluated by PCR and TUNEL methods, respectively. Plasma levels of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were studied by the ELISA method and tissue samples were examined histopathologically as well. RESULTS: Anakinra inhibited the expression of IL-1α, IL-6, and TNF-α and decreased the SOD, CAT, and MDA caused by ischemia-reperfusion injury in both treatment groups. Caspase-3 expression and TUNEL-positive cell number in treatment groups were also less. Histopathologically, anakinra better preserved the villous structure of the small intestine at a dose of 100 mg/kg than 50 mg/kg. CONCLUSION: Anakinra decreased the intestinal damage caused by ischemia-reperfusion and a dose of 100 mg/kg was found to be histopathologically more effective. The Scientific and Technological Research Council of Turkey 2021-08-30 /pmc/articles/PMC8569752/ /pubmed/33843175 http://dx.doi.org/10.3906/sag-2008-258 Text en Copyright © 2021 The Author(s) https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Article KANDEMİR, Muhammed YAŞAR, Necdet Fatih ÖZKURT, Mete ÖZYURT, Rumeysa BEKTUR AYKANAT, Nuriye Ezgi ERKASAP, Nilüfer The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title | The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title_full | The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title_fullStr | The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title_full_unstemmed | The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title_short | The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
title_sort | role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8569752/ https://www.ncbi.nlm.nih.gov/pubmed/33843175 http://dx.doi.org/10.3906/sag-2008-258 |
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