NDLI: Astaxanthin alleviates spinal cord ischemia-reperfusion injury via activation of PI3K/Akt/GSK-3β pathway in rats

Content Provider	Springer Nature : BioMed Central
Author	Fu, Jian Sun, Haibin Wei, Haofei Dong, Mingjie Zhang, Yongzhe Xu, Wei Fang, Yanwei Zhao, Jianhui
Abstract	Background Ischemia-reperfusion injury of the spinal cord (SCII) often leads to unalterable neurological deficits, which may be associated with apoptosis induced by oxidative stress and inflammation. Astaxanthin (AST) is a strong antioxidant and anti-inflammatory agent with multitarget neuroprotective effects. This study aimed to investigate the potential therapeutic effects of AST for SCII and the molecular mechanism. Methods Rat models of SCII with abdominal aortic occlusion for 40 min were carried out to investigate the effects of AST on the recovery of SCII. Tarlov’s scores were used to assess the neuronal function; HE and TUNEL staining were used to observe the pathological morphology of lesions. Neuron oxidative stress and inflammation were measured using commercial detection kits. Flow cytometry was conducted to assess the mitochondrial swelling degree. Besides, Western blot assay was used to detect the expression of PI3K/Akt/GSK-3β pathway-related proteins, as well as NOX2 and NLRP3 proteins. Results The results demonstrated that AST pretreatment promoted the hind limb motor function recovery and alleviated the pathological damage induced by SCII. Moreover, AST significantly enhanced the antioxidative stress response and attenuated mitochondrial swelling. However, AST pretreatment hardly inhibited the levels of proinflammatory cytokines after SCII. Most importantly, AST activated p-Akt and p-GSK-3β expression levels. Meanwhile, cotreatment with LY294002 (a PI3K inhibitor) was found to abolish the above protective effects observed with the AST pretreatment. Conclusion Overall, these results suggest that AST pretreatment not only mitigates pathological tissue damage but also effectively improves neural functional recovery following SCII, primarily by alleviating oxidative stress but not inhibiting inflammation. A possible underlying molecular mechanism of AST may be mainly attributed to the activation of PI3K/Akt/GSK-3β pathway.
Related Links	https://josr-online.biomedcentral.com/counter/pdf/10.1186/s13018-020-01790-8.pdf
Ending Page	11
Page Count	11
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s13018-020-01790-8
Journal	Journal of Orthopaedic Surgery and Research
Issue Number	1
Volume Number	15
Language	English
Publisher	BioMed Central
Publisher Date	2020-07-23
Access Restriction	Open
Subject Keyword	Orthopedics Surgical Orthopedics Spinal cord ischemia-reperfusion injury Astaxanthin Oxidative stress Inflammation Apoptosis Mitochondria swelling
Content Type	Text
Resource Type	Article
Subject	Surgery Orthopedics and Sports Medicine
Journal Impact Factor	2.8/2023
5-Year Journal Impact Factor	3/2023

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