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.
Highlights
Ischemia reperfusion injury is a secondary pathological condition caused by restoration of blood perfusion to the primary ischemic tissues [1]
Our present results show that the dyskinesia and histopathological deterioration after Spinal cord ischemia/reperfusion (SCI/R) are apparently alleviated by the natural flavonoid astragalin, and we have verified amelioration of astragalin administration to oxidative stress and inflammation, which are similar to the effects of RIP1 inhibitor necrostatin-1
We conclude that astragalin is a protective agent to SCI/R, and the potential cellular mechanism is based on its alleviation to oxidative stress-induced necroptosis
Summary
Ischemia reperfusion injury is a secondary pathological condition caused by restoration of blood perfusion to the primary ischemic tissues [1]. Occurrence of secondary reperfusion injury after surgery is still inevitable, especially in thoracoabdominal aortic surgery. Spinal cord ischemia/reperfusion (SCI/R) injury is mainly such a devastating complication of thoracoabdominal aortic surgery, which will in different degree threaten the patients with risk of quadriplegia or paraplegia [2,3,4]. Excessive reactive oxygen species elicited by ischemia and reperfusion overwhelms the redox balance of cells leading to oxidative stress. Cell necrosis is one of the downstream events of oxidative stress and catastrophic consequence of ischemia reperfusion [1].
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