Abstract |
Spinal cord ischemia/reperfusion (SCI/R) injury is a devastating complication usually occurring after thoracoabdominal aortic surgery. However, it remains unsatisfactory for its intervention by using pharmacological strategies. Oxidative stress is a main pharmacological process involved in SCI/R, which will elicit downstream programmed cell death such as the novel defined necroptosis. Astragalin is a bioactive natural flavonoid with a wide spectrum of pharmacological activities. Herein, we firstly evaluated the effect of astragalin to oxidative stress as well as the possible downstream necroptosis after SCI/R in mice. Our results demonstrated that astragalin improves the ethological score and histopathological deterioration of SCI/R mice. Astragalin mitigates oxidative stress and ameliorates inflammation after SCI/R. Astragalin blocks necroptosis induced by SCI/R. That is, the amelioration of astragalin to the motoneuron injury and histopathological changes. Indicators of oxidative stress, inflammation, and necroptosis after SCI/R were significantly blocked. Summarily, we firstly illustrated the protection of astragalin against SCI/R through its blockage to the necroptosis at downstream of oxidative stress.
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Authors | Feng Sun, Haiwei Zhang, Jianhui Shi, Tianwen Huang, Yansong Wang |
Journal | BioMed research international
(Biomed Res Int)
Vol. 2021
Pg. 7254708
( 2021)
ISSN: 2314-6141 [Electronic] United States |
PMID | 34746308
(Publication Type: Journal Article, Retracted Publication)
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Copyright | Copyright © 2021 Feng Sun et al. |
Chemical References |
- Antioxidants
- Flavonoids
- Kaempferols
- Neuroprotective Agents
- astragalin
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Topics |
- Animals
- Antioxidants
(metabolism)
- Apoptosis
(drug effects)
- Flavonoids
(pharmacology)
- Inflammation
(drug therapy)
- Kaempferols
(metabolism, pharmacology)
- Male
- Mice
- Mice, Inbred C57BL
- Models, Animal
- Necroptosis
(drug effects, physiology)
- Neuroprotective Agents
(pharmacology)
- Oxidative Stress
(drug effects, physiology)
- Reperfusion Injury
(drug therapy, metabolism)
- Spinal Cord
(physiopathology)
- Spinal Cord Injuries
(physiopathology)
- Spinal Cord Ischemia
(complications, drug therapy, physiopathology)
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