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Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation
INTRODUCTION: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anti-cancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127787/ https://www.ncbi.nlm.nih.gov/pubmed/32280228 http://dx.doi.org/10.2147/NDT.S227988 |
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author | Zhang, Yi Tian, Zhiming Wan, Hongyan Liu, Wen Kong, Fanping Ma, Guoping |
author_facet | Zhang, Yi Tian, Zhiming Wan, Hongyan Liu, Wen Kong, Fanping Ma, Guoping |
author_sort | Zhang, Yi |
collection | PubMed |
description | INTRODUCTION: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anti-cancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate the role of deltonin in cerebral ischemia/reperfusion injuries. METHODS: Ly294002 and anisomycin were used as inhibitors to monitor the effects of deltonin. Middle cerebral artery occlusion I/R model was constructed. Infarct volumes, neurological deficits and brain water contents were evaluated under different conditions. Rotarod test, ELISA, and Western blotting were carried to investigate the effects in vitro. RESULTS: We found that deltonin in ischemia/reperfusion (I/R) rats greatly enhanced brain damages as well as neurological functions through up-regulating p-Akt and p-mTOR as well as inhibiting the expressions of LC3-II/LC3-I, Beclin-1, IL-1, TLR4, and p-p38. Deltonin exerted neuroprotection effect through relieving autophagy activity by regulating PI3K/Akt/mTOR signaling. Deltonin suppressed inflammation reactions through modulation TLR4/p38/MAPK signaling as well. CONCLUSION: Overall, our data suggested that deltonin could suppress ischemic brain injury by regulating autophagy and inflammation during I/R. Deltonin can be a potential therapeutic method for patient with I/R. |
format | Online Article Text |
id | pubmed-7127787 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-71277872020-04-10 Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation Zhang, Yi Tian, Zhiming Wan, Hongyan Liu, Wen Kong, Fanping Ma, Guoping Neuropsychiatr Dis Treat Original Research INTRODUCTION: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anti-cancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate the role of deltonin in cerebral ischemia/reperfusion injuries. METHODS: Ly294002 and anisomycin were used as inhibitors to monitor the effects of deltonin. Middle cerebral artery occlusion I/R model was constructed. Infarct volumes, neurological deficits and brain water contents were evaluated under different conditions. Rotarod test, ELISA, and Western blotting were carried to investigate the effects in vitro. RESULTS: We found that deltonin in ischemia/reperfusion (I/R) rats greatly enhanced brain damages as well as neurological functions through up-regulating p-Akt and p-mTOR as well as inhibiting the expressions of LC3-II/LC3-I, Beclin-1, IL-1, TLR4, and p-p38. Deltonin exerted neuroprotection effect through relieving autophagy activity by regulating PI3K/Akt/mTOR signaling. Deltonin suppressed inflammation reactions through modulation TLR4/p38/MAPK signaling as well. CONCLUSION: Overall, our data suggested that deltonin could suppress ischemic brain injury by regulating autophagy and inflammation during I/R. Deltonin can be a potential therapeutic method for patient with I/R. Dove 2020-03-31 /pmc/articles/PMC7127787/ /pubmed/32280228 http://dx.doi.org/10.2147/NDT.S227988 Text en © 2020 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhang, Yi Tian, Zhiming Wan, Hongyan Liu, Wen Kong, Fanping Ma, Guoping Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title | Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title_full | Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title_fullStr | Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title_full_unstemmed | Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title_short | Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation with Modulation of Autophagy and Inflammation |
title_sort | deltonin ameliorates cerebral ischemia/reperfusion injury in correlation with modulation of autophagy and inflammation |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127787/ https://www.ncbi.nlm.nih.gov/pubmed/32280228 http://dx.doi.org/10.2147/NDT.S227988 |
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