Cargando…

YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis

YiQiFuMai (YQFM) powder injection as a modern preparation derived from Sheng Mai San, a traditional Chinese medicine, has been widely used in the treatment of cardiovascular and cerebrovascular diseases. However, its neuroprotective effect and underlying mechanism in cerebral ischemia remain to be e...

Descripción completa

Detalles Bibliográficos
Autores principales: Cao, Guosheng, Zhou, Huana, Jiang, Nan, Han, Yuwei, Hu, Yang, Zhang, Yuanyuan, Qi, Jin, Kou, Junping, Yu, Boyang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818822/
https://www.ncbi.nlm.nih.gov/pubmed/27087890
http://dx.doi.org/10.1155/2016/5493279
_version_ 1782425090039742464
author Cao, Guosheng
Zhou, Huana
Jiang, Nan
Han, Yuwei
Hu, Yang
Zhang, Yuanyuan
Qi, Jin
Kou, Junping
Yu, Boyang
author_facet Cao, Guosheng
Zhou, Huana
Jiang, Nan
Han, Yuwei
Hu, Yang
Zhang, Yuanyuan
Qi, Jin
Kou, Junping
Yu, Boyang
author_sort Cao, Guosheng
collection PubMed
description YiQiFuMai (YQFM) powder injection as a modern preparation derived from Sheng Mai San, a traditional Chinese medicine, has been widely used in the treatment of cardiovascular and cerebrovascular diseases. However, its neuroprotective effect and underlying mechanism in cerebral ischemia remain to be explored. The present study was designed to investigate the neuroprotective effect of YQFM on endoplasmic reticulum (ER) stress-mediated neuronal apoptosis in the permanent middle cerebral artery occlusion- (MCAO-) injured mice and the oxygen-glucose deprivation- (OGD-) induced pheochromocytoma (PC12) cells. The results showed that single administration of YQFM (1.342 g/kg, i.p.) could reduce the brain infarction and improve the neurological deficits and the cerebral blood flow (CBF) after MCAO for 24 h in mice. Moreover, incubation with YQFM (100, 200, and 400 μg/mL) could increase the cell viability, decrease the caspase-3 activity, and inhibit the cell apoptosis in OGD-induced PC12 cells for 12 h. In addition, YQFM treatment could significantly modulate cleaved caspase-3 and Bcl-2 expressions and inhibit the expressions of ER stress-related marker proteins and signaling pathways in vivo and in vitro. In conclusion, our findings provide the first evidence that YQFM ameliorates cerebral ischemic injury linked with modulating ER stress-related signaling pathways, which provided some new insights for its prevention and treatment of cerebral ischemia diseases.
format Online
Article
Text
id pubmed-4818822
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-48188222016-04-17 YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis Cao, Guosheng Zhou, Huana Jiang, Nan Han, Yuwei Hu, Yang Zhang, Yuanyuan Qi, Jin Kou, Junping Yu, Boyang Oxid Med Cell Longev Research Article YiQiFuMai (YQFM) powder injection as a modern preparation derived from Sheng Mai San, a traditional Chinese medicine, has been widely used in the treatment of cardiovascular and cerebrovascular diseases. However, its neuroprotective effect and underlying mechanism in cerebral ischemia remain to be explored. The present study was designed to investigate the neuroprotective effect of YQFM on endoplasmic reticulum (ER) stress-mediated neuronal apoptosis in the permanent middle cerebral artery occlusion- (MCAO-) injured mice and the oxygen-glucose deprivation- (OGD-) induced pheochromocytoma (PC12) cells. The results showed that single administration of YQFM (1.342 g/kg, i.p.) could reduce the brain infarction and improve the neurological deficits and the cerebral blood flow (CBF) after MCAO for 24 h in mice. Moreover, incubation with YQFM (100, 200, and 400 μg/mL) could increase the cell viability, decrease the caspase-3 activity, and inhibit the cell apoptosis in OGD-induced PC12 cells for 12 h. In addition, YQFM treatment could significantly modulate cleaved caspase-3 and Bcl-2 expressions and inhibit the expressions of ER stress-related marker proteins and signaling pathways in vivo and in vitro. In conclusion, our findings provide the first evidence that YQFM ameliorates cerebral ischemic injury linked with modulating ER stress-related signaling pathways, which provided some new insights for its prevention and treatment of cerebral ischemia diseases. Hindawi Publishing Corporation 2016 2016-03-20 /pmc/articles/PMC4818822/ /pubmed/27087890 http://dx.doi.org/10.1155/2016/5493279 Text en Copyright © 2016 Guosheng Cao et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Cao, Guosheng
Zhou, Huana
Jiang, Nan
Han, Yuwei
Hu, Yang
Zhang, Yuanyuan
Qi, Jin
Kou, Junping
Yu, Boyang
YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title_full YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title_fullStr YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title_full_unstemmed YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title_short YiQiFuMai Powder Injection Ameliorates Cerebral Ischemia by Inhibiting Endoplasmic Reticulum Stress-Mediated Neuronal Apoptosis
title_sort yiqifumai powder injection ameliorates cerebral ischemia by inhibiting endoplasmic reticulum stress-mediated neuronal apoptosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818822/
https://www.ncbi.nlm.nih.gov/pubmed/27087890
http://dx.doi.org/10.1155/2016/5493279
work_keys_str_mv AT caoguosheng yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT zhouhuana yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT jiangnan yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT hanyuwei yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT huyang yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT zhangyuanyuan yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT qijin yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT koujunping yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis
AT yuboyang yiqifumaipowderinjectionamelioratescerebralischemiabyinhibitingendoplasmicreticulumstressmediatedneuronalapoptosis