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Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats
Renal ischemia-reperfusion (IR) causes remote liver damage. Oxytocin has anti-inflammatory and antioxidant effects. The main purpose of this study was to evaluate the protective function of oxytocin (OT) in remote liver damage triggered by renal IR in rats. Twenty four rats were randomly divided int...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Physiological Society and The Korean Society of Pharmacology
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634095/ https://www.ncbi.nlm.nih.gov/pubmed/23626480 http://dx.doi.org/10.4196/kjpp.2013.17.2.169 |
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author | Tas Hekimoglu, Askın Toprak, Gulten Akkoc, Hasan Evliyaoglu, Osman Ozekinci, Selver Kelle, Ilker |
author_facet | Tas Hekimoglu, Askın Toprak, Gulten Akkoc, Hasan Evliyaoglu, Osman Ozekinci, Selver Kelle, Ilker |
author_sort | Tas Hekimoglu, Askın |
collection | PubMed |
description | Renal ischemia-reperfusion (IR) causes remote liver damage. Oxytocin has anti-inflammatory and antioxidant effects. The main purpose of this study was to evaluate the protective function of oxytocin (OT) in remote liver damage triggered by renal IR in rats. Twenty four rats were randomly divided into four different groups, each containing 8 rats. The groups were as follows: (1) Sham operated group; (2) Sham operated+OT group (3) Renal IR group; (4) Renal IR+OT group. OT (500µg/kg) was administered subcutaneously 12 and 24 hours before and immediately after ischemia. At the end of experimental procedure, the rats were sacrificed, and liver specimens were taken for histological assessment or determination of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), paraoxonase (PON-1) activity and nitric oxide (NO). The results showed that renal IR injury constituted a notable elevation in MDA, TOS, Oxidative stress index (OSI) and significantly decreased TAS, PON-1 actvity and NO in liver tissue (p<0.05). Additionally renal IR provoked significant augmentation in hepatic microscopic damage scores. However, alterations in these biochemical and histopathological indices due to IR injury were attenuated by OT treatment (p<0.05). These findings show that OT ameliorates remote liver damage triggered by renal ischemia-reperfusion and this preservation involves suppression of inflammation and regulation of oxidant-antioxidant status. |
format | Online Article Text |
id | pubmed-3634095 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The Korean Physiological Society and The Korean Society of Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-36340952013-04-26 Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats Tas Hekimoglu, Askın Toprak, Gulten Akkoc, Hasan Evliyaoglu, Osman Ozekinci, Selver Kelle, Ilker Korean J Physiol Pharmacol Original Article Renal ischemia-reperfusion (IR) causes remote liver damage. Oxytocin has anti-inflammatory and antioxidant effects. The main purpose of this study was to evaluate the protective function of oxytocin (OT) in remote liver damage triggered by renal IR in rats. Twenty four rats were randomly divided into four different groups, each containing 8 rats. The groups were as follows: (1) Sham operated group; (2) Sham operated+OT group (3) Renal IR group; (4) Renal IR+OT group. OT (500µg/kg) was administered subcutaneously 12 and 24 hours before and immediately after ischemia. At the end of experimental procedure, the rats were sacrificed, and liver specimens were taken for histological assessment or determination of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), paraoxonase (PON-1) activity and nitric oxide (NO). The results showed that renal IR injury constituted a notable elevation in MDA, TOS, Oxidative stress index (OSI) and significantly decreased TAS, PON-1 actvity and NO in liver tissue (p<0.05). Additionally renal IR provoked significant augmentation in hepatic microscopic damage scores. However, alterations in these biochemical and histopathological indices due to IR injury were attenuated by OT treatment (p<0.05). These findings show that OT ameliorates remote liver damage triggered by renal ischemia-reperfusion and this preservation involves suppression of inflammation and regulation of oxidant-antioxidant status. The Korean Physiological Society and The Korean Society of Pharmacology 2013-04 2013-04-10 /pmc/articles/PMC3634095/ /pubmed/23626480 http://dx.doi.org/10.4196/kjpp.2013.17.2.169 Text en Copyright © 2013 The Korean Physiological Society and The Korean Society of Pharmacology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Tas Hekimoglu, Askın Toprak, Gulten Akkoc, Hasan Evliyaoglu, Osman Ozekinci, Selver Kelle, Ilker Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title | Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title_full | Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title_fullStr | Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title_full_unstemmed | Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title_short | Oxytocin Ameliorates Remote Liver Injury Induced by Renal Ischemia-Reperfusion in Rats |
title_sort | oxytocin ameliorates remote liver injury induced by renal ischemia-reperfusion in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634095/ https://www.ncbi.nlm.nih.gov/pubmed/23626480 http://dx.doi.org/10.4196/kjpp.2013.17.2.169 |
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