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Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats
Introduction: Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI). Objectives: This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI. Materials an...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nickan Research Institute
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827383/ https://www.ncbi.nlm.nih.gov/pubmed/27069965 http://dx.doi.org/10.15171/jrip.2016.07 |
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author | Kanani, Fatemeh Fazelnia, Faezeh Mojarradfard, Mohaddeseh Nematbakhsh, Mehdi Moslemi, Fatemeh Eshraghi-Jazi, Fatemeh Talebi, Ardeshir |
author_facet | Kanani, Fatemeh Fazelnia, Faezeh Mojarradfard, Mohaddeseh Nematbakhsh, Mehdi Moslemi, Fatemeh Eshraghi-Jazi, Fatemeh Talebi, Ardeshir |
author_sort | Kanani, Fatemeh |
collection | PubMed |
description | Introduction: Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI). Objectives: This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI. Materials and Methods: Male Wistar rats were subjected to 45 minutes of bilateral renal ischemia by occlusion of renal vessels of both kidney followed by 24 hours of reperfusion. Prior to renal IRI, the rats received either vehicle (saline, group 2) or SMT (50 mg/kg, group 3), and were compared with the sham-operated animals (group 1). At the end of reperfusion period, the rats were sacrificed for kidney tissue pathology investigation. Results: Serum creatinine (Cr), blood urea nitrogen (BUN), nitrite levels, and kidney weight significantly increased in groups 2 and 3 (P < 0.05). Kidney tissue damage scores in groups 2 and 3 were also higher than that in the sham-operated group (P < 0.05). Conclusion: SMT not only prevent the kidney during IRI, but also promotes kidney function disturbance and severity of renal injury. |
format | Online Article Text |
id | pubmed-4827383 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nickan Research Institute |
record_format | MEDLINE/PubMed |
spelling | pubmed-48273832016-04-11 Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats Kanani, Fatemeh Fazelnia, Faezeh Mojarradfard, Mohaddeseh Nematbakhsh, Mehdi Moslemi, Fatemeh Eshraghi-Jazi, Fatemeh Talebi, Ardeshir J Renal Inj Prev Original Article Introduction: Excessive production of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) is associated in renal ischemia reperfusion injury (IRI). Objectives: This study was designed to investigate the role of S-methylisothiourea (SMT) as selective inhibitor iNOS in renal IRI. Materials and Methods: Male Wistar rats were subjected to 45 minutes of bilateral renal ischemia by occlusion of renal vessels of both kidney followed by 24 hours of reperfusion. Prior to renal IRI, the rats received either vehicle (saline, group 2) or SMT (50 mg/kg, group 3), and were compared with the sham-operated animals (group 1). At the end of reperfusion period, the rats were sacrificed for kidney tissue pathology investigation. Results: Serum creatinine (Cr), blood urea nitrogen (BUN), nitrite levels, and kidney weight significantly increased in groups 2 and 3 (P < 0.05). Kidney tissue damage scores in groups 2 and 3 were also higher than that in the sham-operated group (P < 0.05). Conclusion: SMT not only prevent the kidney during IRI, but also promotes kidney function disturbance and severity of renal injury. Nickan Research Institute 2016-02-28 /pmc/articles/PMC4827383/ /pubmed/27069965 http://dx.doi.org/10.15171/jrip.2016.07 Text en Copyright © 2016 The Author(s); Published by Nickan Research Institute http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Kanani, Fatemeh Fazelnia, Faezeh Mojarradfard, Mohaddeseh Nematbakhsh, Mehdi Moslemi, Fatemeh Eshraghi-Jazi, Fatemeh Talebi, Ardeshir Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title | Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title_full | Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title_fullStr | Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title_full_unstemmed | Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title_short | Role of S-methylisothiourea (SMT) in renal ischemia/reperfusion injury in rats |
title_sort | role of s-methylisothiourea (smt) in renal ischemia/reperfusion injury in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827383/ https://www.ncbi.nlm.nih.gov/pubmed/27069965 http://dx.doi.org/10.15171/jrip.2016.07 |
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