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Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis
BACKGROUND: Studies have demonstrated that allicin may play critical roles in the procession of ischemia–reperfusion(I/R) injury. The purpose of this study was to investigate the protective effects of allicin on renal I/R injury by attenuating oxidative stress and apoptosis. METHODS: To establish a...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9184421/ https://www.ncbi.nlm.nih.gov/pubmed/34825305 http://dx.doi.org/10.1007/s11255-021-03014-2 |
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author | Li, Maolin Ning, Jinzhuo Huang, Houbao Jiang, Shuchuan Zhuo, Dong |
author_facet | Li, Maolin Ning, Jinzhuo Huang, Houbao Jiang, Shuchuan Zhuo, Dong |
author_sort | Li, Maolin |
collection | PubMed |
description | BACKGROUND: Studies have demonstrated that allicin may play critical roles in the procession of ischemia–reperfusion(I/R) injury. The purpose of this study was to investigate the protective effects of allicin on renal I/R injury by attenuating oxidative stress and apoptosis. METHODS: To establish a model of renal I/R, the right kidney underwent 12 h reperfusion after 45 min ischemia, allicin was administered intraperitoneally at concentrations of 40, 50 or 60 mg/kg. NRK-52E cells were treated with allicin at concentrations of 1, 3 or 5 μM in 24 h hypoxia/ 6 h reoxygenation(H/R) treatments. Indicators of HE, oxidative stress, apoptosis were measured to evaluate the effect of aliicin on renal I/R injury. RESULTS: Allicin protected renal I/R injury by ameliorating histological injury and decreasing the oxidative stress in renal tissues. Meanwhile, allicin significantly downregulated the expression of Bax and caspase-3, upregulated the expression of Bcl-2 in I/R renal tissues and H/R treated NRK-52E cells. CONCLUSIONS: Allicin may exert anti-apoptotic and antioxidative effects to promote renal function recovery in I/R renal tissues and H/R treated NRK-52E cells. Taken together, allicin may be a potential novel therapy option for future renal injury protection. |
format | Online Article Text |
id | pubmed-9184421 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-91844212022-06-11 Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis Li, Maolin Ning, Jinzhuo Huang, Houbao Jiang, Shuchuan Zhuo, Dong Int Urol Nephrol Nephrology - Original Paper BACKGROUND: Studies have demonstrated that allicin may play critical roles in the procession of ischemia–reperfusion(I/R) injury. The purpose of this study was to investigate the protective effects of allicin on renal I/R injury by attenuating oxidative stress and apoptosis. METHODS: To establish a model of renal I/R, the right kidney underwent 12 h reperfusion after 45 min ischemia, allicin was administered intraperitoneally at concentrations of 40, 50 or 60 mg/kg. NRK-52E cells were treated with allicin at concentrations of 1, 3 or 5 μM in 24 h hypoxia/ 6 h reoxygenation(H/R) treatments. Indicators of HE, oxidative stress, apoptosis were measured to evaluate the effect of aliicin on renal I/R injury. RESULTS: Allicin protected renal I/R injury by ameliorating histological injury and decreasing the oxidative stress in renal tissues. Meanwhile, allicin significantly downregulated the expression of Bax and caspase-3, upregulated the expression of Bcl-2 in I/R renal tissues and H/R treated NRK-52E cells. CONCLUSIONS: Allicin may exert anti-apoptotic and antioxidative effects to promote renal function recovery in I/R renal tissues and H/R treated NRK-52E cells. Taken together, allicin may be a potential novel therapy option for future renal injury protection. Springer Netherlands 2021-11-25 2022 /pmc/articles/PMC9184421/ /pubmed/34825305 http://dx.doi.org/10.1007/s11255-021-03014-2 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Nephrology - Original Paper Li, Maolin Ning, Jinzhuo Huang, Houbao Jiang, Shuchuan Zhuo, Dong Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title | Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title_full | Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title_fullStr | Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title_full_unstemmed | Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title_short | Allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
title_sort | allicin protects against renal ischemia–reperfusion injury by attenuating oxidative stress and apoptosis |
topic | Nephrology - Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9184421/ https://www.ncbi.nlm.nih.gov/pubmed/34825305 http://dx.doi.org/10.1007/s11255-021-03014-2 |
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