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Abstract Title:

Effect of astaxanthin on neuron damage, inflammatory factors expressions and oxidative stress in mice with subarachnoid hemorrhage.

Abstract Source:

Am J Transl Res. 2021 ;13(11):13043-13050. Epub 2021 Nov 15. PMID: 34956522

Abstract Author(s):

Yu Qian, Xinyu Lu, Lulu Chen, Jinyu Sun, Kan Cao, Qiang Yu, Junfei Shao

Article Affiliation:

Yu Qian

Abstract:

OBJECTIVE: This study aimed to explore the effect of astaxanthin (ATX) on neuron damage, inflammatory factor expression and oxidative stress in mice with subarachnoid hemorrhage (SAH).

METHODS: Specific-pathogen-free, 'Institute of Cancer Research', male mice were randomly divided into four groups: SAH group, sham group, SAH + placebo group (SAH + Vehicle group) and SAH + ATX group. Neurological function was scored in each group. Brain water content, reactive oxygen species (ROS) content and inflammatory factor levels in the brain were detected by wet-dry weighting method, DCFH-DA fluorescent probe staining method and ELISA, respectively. Expression of NADPH oxidase 2 (NOX2), glial fibrillary acidic protein (GFAP) and apoptosis-related proteins Bax and Bcl-2 were detected by Western blot and quantitative real-time polymerase chain reaction. Neuronal apoptosis was detected by TUNEL staining.

RESULTS: Compared with sham group, neurological score, brain water content and ROS content in the other three groups increased significantly (all P<0.05). Neurological score, brain water content and ROS content in SAH + ATX group were lower than those in SAH group (all P<0.05). Compared with the sham group, there was increased expression of interleukin (IL)-6, IL-17 and tumor necrosis factorα (TNF-α), and increased neuronal apoptosis, as well as enhanced expression of NOX2, GFAP and Bax; while there was decreased IL-10 expression, and declined Bcl-2 expression, in the other three groups (all P<0.05). There was decreased expression of IL-6, IL-17 and TNF-α, declined expressions of NOX2, GFAP and Bax, and lowered neuronal apoptosis; while there was increased IL-10 expression, and enhanced Bcl-2 expression, in SAH + ATX group as compared to SAH group (all P<0.05). All indicators between SAH group and SAH + Vehicle group showed no significant differences (all P>0.05).

CONCLUSION: Astaxanthin can decrease neuron damage, inhibit inflammatory response, and improve oxidative stress in SAH mice. Thus, astaxanthin is a method for treating SAH.

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