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Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway
Cerebral stroke is a kind of acute cerebrovascular disease with high incidence, morbidity and disability. Treatments against various types of cerebral stroke are limited at preventive measurements due to the lack of effective therapeutic method. The present study aimed to investigate the protective...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779989/ https://www.ncbi.nlm.nih.gov/pubmed/29152647 http://dx.doi.org/10.3892/mmr.2017.7824 |
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author | Zhu, Weixin Qiu, Weihong Lu, Ailan |
author_facet | Zhu, Weixin Qiu, Weihong Lu, Ailan |
author_sort | Zhu, Weixin |
collection | PubMed |
description | Cerebral stroke is a kind of acute cerebrovascular disease with high incidence, morbidity and disability. Treatments against various types of cerebral stroke are limited at preventive measurements due to the lack of effective therapeutic method. The present study aimed to investigate the protective effect of cryptotanshinone (CPT) on cerebral stroke, and investigate the possible mechanism involved in order to develop a novel therapy against stoke. The phosphoinositide 3-kinase membrane translocation of cerebral stroke rats pretreated with CPT at various concentrations were measured, as well as the phosphorylation of protein kinase B (AKT) and endothelial nitric oxide synthase (eNOS). Additionally, the expression level of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and vascular endothelial growth factor were also assessed using western blotting and reverse transcription-quantitative polymerase chain reaction. Furthermore, biochemical tests were used to measure the activity of superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) in both the cerebral cortex and peripheral blood. As a result, CPT-pretreated rats presented declined phosphoinositide 3-kinase (PI3K) and AKT expression levels, indicating that the PI3K/AKT signaling pathway was inhibited. Increased Bcl-2 and NO levels in both the cerebral cortex and peripheral blood demonstrated the anti-apoptosis and blood vessel protection effect of CPT. Furthermore, increased SOD activity and declined MDA levels demonstrated suppressed lipid peroxidation. In conclusion, CPT exhibited a protective effect against cerebral stroke through inhibition of the PI3K/AKT-eNOS signaling pathway. These results suggested the potential of CPT as a promising agent in the treatment of cerebral stroke. |
format | Online Article Text |
id | pubmed-5779989 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57799892018-12-01 Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway Zhu, Weixin Qiu, Weihong Lu, Ailan Mol Med Rep Articles Cerebral stroke is a kind of acute cerebrovascular disease with high incidence, morbidity and disability. Treatments against various types of cerebral stroke are limited at preventive measurements due to the lack of effective therapeutic method. The present study aimed to investigate the protective effect of cryptotanshinone (CPT) on cerebral stroke, and investigate the possible mechanism involved in order to develop a novel therapy against stoke. The phosphoinositide 3-kinase membrane translocation of cerebral stroke rats pretreated with CPT at various concentrations were measured, as well as the phosphorylation of protein kinase B (AKT) and endothelial nitric oxide synthase (eNOS). Additionally, the expression level of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and vascular endothelial growth factor were also assessed using western blotting and reverse transcription-quantitative polymerase chain reaction. Furthermore, biochemical tests were used to measure the activity of superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) in both the cerebral cortex and peripheral blood. As a result, CPT-pretreated rats presented declined phosphoinositide 3-kinase (PI3K) and AKT expression levels, indicating that the PI3K/AKT signaling pathway was inhibited. Increased Bcl-2 and NO levels in both the cerebral cortex and peripheral blood demonstrated the anti-apoptosis and blood vessel protection effect of CPT. Furthermore, increased SOD activity and declined MDA levels demonstrated suppressed lipid peroxidation. In conclusion, CPT exhibited a protective effect against cerebral stroke through inhibition of the PI3K/AKT-eNOS signaling pathway. These results suggested the potential of CPT as a promising agent in the treatment of cerebral stroke. D.A. Spandidos 2017-12 2017-10-19 /pmc/articles/PMC5779989/ /pubmed/29152647 http://dx.doi.org/10.3892/mmr.2017.7824 Text en Copyright © 2017, Spandidos Publications |
spellingShingle | Articles Zhu, Weixin Qiu, Weihong Lu, Ailan Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title | Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title_full | Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title_fullStr | Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title_full_unstemmed | Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title_short | Cryptotanshinone exhibits therapeutical effects on cerebral stroke through the PI3K/AKT-eNOS signaling pathway |
title_sort | cryptotanshinone exhibits therapeutical effects on cerebral stroke through the pi3k/akt-enos signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779989/ https://www.ncbi.nlm.nih.gov/pubmed/29152647 http://dx.doi.org/10.3892/mmr.2017.7824 |
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