Yu Qian1,2, Xinyu Lu2, Lulu Chen3, Jinyu Sun3, Kan Cao2, Qiang Yu2, Junfei Shao1. 1. Department of Neurosurgery, Nanjing Medical University Affiliated Wuxi People's Hospital Wuxi 214023, Jiangsu Province, China. 2. Department of Neurosurgery, Jiangsu University Affiliated People's Hospital Zhenjiang 212000, Jiangsu Province, China. 3. Department of Anatomy, Histology and Embryology, Nanjing Medical University Nanjing 211166, Jiangsu Province, China.
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 factor α (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. AJTR
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 factor α (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. AJTR