Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy
Joint Authors
Luo, Yongjun
Kong, Fan-Qi
Gu, Changjiang
Li, Linwei
Huang, Yifan
Qian, Dingfei
Liu, Wei
Zhang, Chengliang
Zhou, Zheng
Zhao, Xuan
Liu, Hao
Gao, Peng
Chen, Jian
Yin, Guoyong
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-22, 22 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-07-23
Country of Publication
Egypt
No. of Pages
22
Main Subjects
Abstract EN
Ischemia-reperfusion injury is the second most common injury of the spinal cord and has the risk of neurological dysfunction and paralysis, which can seriously affect patient quality of life.
Salidroside (Sal) is an active ingredient extracted from Herba Cistanche with a variety of biological attributes such as antioxidant, antiapoptotic, and neuroprotective activities.
Moreover, Sal has shown a protective effect in ischemia-reperfusion injury of the liver, heart, and brain, but its effect in ischemia-reperfusion injury of the spinal cord has not been elucidated.
Here, we demonstrated for the first time that Sal pretreatment can significantly improve functional recovery in mice after spinal cord ischemia-reperfusion injury and significantly inhibit the apoptosis of neurons both in vivo and in vitro.
Neurons have a high metabolic rate, and consequently, mitochondria, as the main energy-supplying suborganelles, become the main injury site of spinal cord ischemia-reperfusion injury.
Mitochondrial pathway-dependent neuronal apoptosis is increasingly confirmed by researchers; therefore, Sal’s effect on mitochondria naturally attracted our attention.
By means of a range of experiments both in vivo and in vitro, we found that Sal can reduce reactive oxygen species production through antioxidant stress to reduce mitochondrial permeability and mitochondrial damage, and it can also enhance the PINK1-Parkin signaling pathway and promote mitophagy to eliminate damaged mitochondria.
In conclusion, our results show that Sal is beneficial to the protection of spinal cord neurons after ischemia-reperfusion injury, mainly by reducing apoptosis associated with the mitochondrial-dependent pathway, among which Sal’s antioxidant and autophagy-promoting properties play an important role.
American Psychological Association (APA)
Gu, Changjiang& Li, Linwei& Huang, Yifan& Qian, Dingfei& Liu, Wei& Zhang, Chengliang…[et al.]. 2020. Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-22.
https://search.emarefa.net/detail/BIM-1204283
Modern Language Association (MLA)
Gu, Changjiang…[et al.]. Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-22.
https://search.emarefa.net/detail/BIM-1204283
American Medical Association (AMA)
Gu, Changjiang& Li, Linwei& Huang, Yifan& Qian, Dingfei& Liu, Wei& Zhang, Chengliang…[et al.]. Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-22.
https://search.emarefa.net/detail/BIM-1204283
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204283