YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission
YiQiFuMai (YQFM) powder injection has been reported to be used in cardiovascular and nervous system diseases with marked efficacy. However, as a treatment against diseases characterized by hypoxia, lassitude, and asthenia, the effects and underlying mechanisms of YQFM in neuronal mitochondrial funct...
Main Authors: | , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Hindawi Limited
2017-01-01
|
Series: | Oxidative Medicine and Cellular Longevity |
Online Access: | http://dx.doi.org/10.1155/2017/1832093 |
id |
doaj-5bd7f64039e448a3af9d10028f7253b8 |
---|---|
record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yingqiong Xu Yan Wang Guangyun Wang Xinyi Ye Jiangwei Zhang Guosheng Cao Yazheng Zhao Zhen Gao Yuanyuan Zhang Boyang Yu Junping Kou |
spellingShingle |
Yingqiong Xu Yan Wang Guangyun Wang Xinyi Ye Jiangwei Zhang Guosheng Cao Yazheng Zhao Zhen Gao Yuanyuan Zhang Boyang Yu Junping Kou YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission Oxidative Medicine and Cellular Longevity |
author_facet |
Yingqiong Xu Yan Wang Guangyun Wang Xinyi Ye Jiangwei Zhang Guosheng Cao Yazheng Zhao Zhen Gao Yuanyuan Zhang Boyang Yu Junping Kou |
author_sort |
Yingqiong Xu |
title |
YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission |
title_short |
YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission |
title_full |
YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission |
title_fullStr |
YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission |
title_full_unstemmed |
YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission |
title_sort |
yiqifumai powder injection protects against ischemic stroke via inhibiting neuronal apoptosis and pkcδ/drp1-mediated excessive mitochondrial fission |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2017-01-01 |
description |
YiQiFuMai (YQFM) powder injection has been reported to be used in cardiovascular and nervous system diseases with marked efficacy. However, as a treatment against diseases characterized by hypoxia, lassitude, and asthenia, the effects and underlying mechanisms of YQFM in neuronal mitochondrial function and dynamics have not been fully elucidated. Here, we demonstrated that YQFM inhibited mitochondrial apoptosis and activation of dynamin-related protein 1 (Drp1) in cerebral ischemia-injured rats, producing a significant improvement in cerebral infarction and neurological score. YQFM also attenuated oxidative stress-induced mitochondrial dysfunction and apoptosis through increasing ATP level and mitochondria membrane potential (Δψm), inhibiting ROS production, and regulating Bcl-2 family protein levels in primary cultured neurons. Moreover, YQFM inhibited excessive mitochondrial fission, Drp1 phosphorylation, and translocation from cytoplasm to mitochondria induced by oxidative stress. We provided the first evidence that YQFM inhibited the activation, association, and translocation of PKCδ and Drp1 upon oxidative stress. Taken together, we demonstrate that YQFM ameliorates ischemic stroke-induced neuronal apoptosis through inhibiting mitochondrial dysfunction and PKCδ/Drp1-mediated excessive mitochondrial fission. These findings not only put new insights into the unique neuroprotective properties of YQFM associated with the regulation of mitochondrial function but also expand our understanding of the underlying mechanisms of ischemic stroke. |
url |
http://dx.doi.org/10.1155/2017/1832093 |
work_keys_str_mv |
AT yingqiongxu yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT yanwang yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT guangyunwang yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT xinyiye yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT jiangweizhang yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT guoshengcao yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT yazhengzhao yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT zhengao yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT yuanyuanzhang yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT boyangyu yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission AT junpingkou yiqifumaipowderinjectionprotectsagainstischemicstrokeviainhibitingneuronalapoptosisandpkcddrp1mediatedexcessivemitochondrialfission |
_version_ |
1725625442975612928 |
spelling |
doaj-5bd7f64039e448a3af9d10028f7253b82020-11-24T23:05:50ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942017-01-01201710.1155/2017/18320931832093YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial FissionYingqiong Xu0Yan Wang1Guangyun Wang2Xinyi Ye3Jiangwei Zhang4Guosheng Cao5Yazheng Zhao6Zhen Gao7Yuanyuan Zhang8Boyang Yu9Junping Kou10Department of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaDepartment of Complex Prescription of TCM, State Key Laboratory of Natural Products, Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, ChinaYiQiFuMai (YQFM) powder injection has been reported to be used in cardiovascular and nervous system diseases with marked efficacy. However, as a treatment against diseases characterized by hypoxia, lassitude, and asthenia, the effects and underlying mechanisms of YQFM in neuronal mitochondrial function and dynamics have not been fully elucidated. Here, we demonstrated that YQFM inhibited mitochondrial apoptosis and activation of dynamin-related protein 1 (Drp1) in cerebral ischemia-injured rats, producing a significant improvement in cerebral infarction and neurological score. YQFM also attenuated oxidative stress-induced mitochondrial dysfunction and apoptosis through increasing ATP level and mitochondria membrane potential (Δψm), inhibiting ROS production, and regulating Bcl-2 family protein levels in primary cultured neurons. Moreover, YQFM inhibited excessive mitochondrial fission, Drp1 phosphorylation, and translocation from cytoplasm to mitochondria induced by oxidative stress. We provided the first evidence that YQFM inhibited the activation, association, and translocation of PKCδ and Drp1 upon oxidative stress. Taken together, we demonstrate that YQFM ameliorates ischemic stroke-induced neuronal apoptosis through inhibiting mitochondrial dysfunction and PKCδ/Drp1-mediated excessive mitochondrial fission. These findings not only put new insights into the unique neuroprotective properties of YQFM associated with the regulation of mitochondrial function but also expand our understanding of the underlying mechanisms of ischemic stroke.http://dx.doi.org/10.1155/2017/1832093 |