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Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke
Recombinant tissue plasminogen activator (rt‐PA) is the first‐line drug for revascularization in acute cerebral infarction (ACI) treatment. In this study, an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke was used and the rats were killed on the first, third and sev...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433693/ https://www.ncbi.nlm.nih.gov/pubmed/30697923 http://dx.doi.org/10.1111/jcmm.14120 |
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author | Si, Zhihua Liu, Jinzhi Hu, Ke Lin, Yan Liu, Jie Wang, Aihua |
author_facet | Si, Zhihua Liu, Jinzhi Hu, Ke Lin, Yan Liu, Jie Wang, Aihua |
author_sort | Si, Zhihua |
collection | PubMed |
description | Recombinant tissue plasminogen activator (rt‐PA) is the first‐line drug for revascularization in acute cerebral infarction (ACI) treatment. In this study, an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke was used and the rats were killed on the first, third and seventh day after model establishment. Increases in infarct volume were significantly less in the thrombolytic group than in the conventional group at every time‐point. The microvascular density (MVD) in the thrombolytic group was significantly higher than that in the conventional group at every time‐point, especially on the seventh day. Increases in the expressions of neuronal nitric‐oxide synthase (NOS) and caspase‐3 in the ischaemic region and in the nitric oxide contents, malondialdehyde contents, and inducible NOS activities in the cortex of infarct side were significantly less in the thrombolytic group than in the conventional group. Furthermore, decreases in the superoxide dismutase activities in the thrombolytic group were significantly less than those in the conventional group. In conclusion, thrombolytic rt‐PA therapy within a broadened therapeutic window (6 hours) could significantly decrease the infarct volume after ACI, possibly by increasing MVD in the ischaemic region, decreasing apoptotic molecule expression, and alleviating the oxidative stress response. |
format | Online Article Text |
id | pubmed-6433693 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64336932019-04-08 Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke Si, Zhihua Liu, Jinzhi Hu, Ke Lin, Yan Liu, Jie Wang, Aihua J Cell Mol Med Original Articles Recombinant tissue plasminogen activator (rt‐PA) is the first‐line drug for revascularization in acute cerebral infarction (ACI) treatment. In this study, an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke was used and the rats were killed on the first, third and seventh day after model establishment. Increases in infarct volume were significantly less in the thrombolytic group than in the conventional group at every time‐point. The microvascular density (MVD) in the thrombolytic group was significantly higher than that in the conventional group at every time‐point, especially on the seventh day. Increases in the expressions of neuronal nitric‐oxide synthase (NOS) and caspase‐3 in the ischaemic region and in the nitric oxide contents, malondialdehyde contents, and inducible NOS activities in the cortex of infarct side were significantly less in the thrombolytic group than in the conventional group. Furthermore, decreases in the superoxide dismutase activities in the thrombolytic group were significantly less than those in the conventional group. In conclusion, thrombolytic rt‐PA therapy within a broadened therapeutic window (6 hours) could significantly decrease the infarct volume after ACI, possibly by increasing MVD in the ischaemic region, decreasing apoptotic molecule expression, and alleviating the oxidative stress response. John Wiley and Sons Inc. 2019-01-29 2019-04 /pmc/articles/PMC6433693/ /pubmed/30697923 http://dx.doi.org/10.1111/jcmm.14120 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Si, Zhihua Liu, Jinzhi Hu, Ke Lin, Yan Liu, Jie Wang, Aihua Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title | Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title_full | Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title_fullStr | Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title_full_unstemmed | Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title_short | Effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
title_sort | effects of thrombolysis within 6 hours on acute cerebral infarction in an improved rat embolic middle cerebral artery occlusion model for ischaemic stroke |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433693/ https://www.ncbi.nlm.nih.gov/pubmed/30697923 http://dx.doi.org/10.1111/jcmm.14120 |
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