Qian Yu, Lu Xinyu, Chen Lulu, Sun Jinyu, Cao Kan, Yu Qiang, Shao Junfei
Department of Neurosurgery, Nanjing Medical University Affiliated Wuxi People's Hospital Wuxi 214023, Jiangsu Province, China.
Department of Neurosurgery, Jiangsu University Affiliated People's Hospital Zhenjiang 212000, Jiangsu Province, China.
Am J Transl Res. 2021 Nov 15;13(11):13043-13050. eCollection 2021.
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).
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.
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).
Astaxanthin can decrease neuron damage, inhibit inflammatory response, and improve oxidative stress in SAH mice. Thus, astaxanthin is a method for treating SAH.
本研究旨在探讨虾青素(ATX)对蛛网膜下腔出血(SAH)小鼠神经元损伤、炎性因子表达及氧化应激的影响。
将无特定病原体的英国癌症研究所雄性小鼠随机分为四组:SAH组、假手术组、SAH + 安慰剂组(SAH + 溶剂组)和SAH + ATX组。对每组小鼠进行神经功能评分。分别采用干湿重法、DCFH-DA荧光探针染色法和ELISA检测脑含水量、活性氧(ROS)含量及脑内炎性因子水平。采用蛋白质免疫印迹法和定量实时聚合酶链反应检测烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NOX2)、胶质纤维酸性蛋白(GFAP)及凋亡相关蛋白Bax和Bcl-2的表达。采用TUNEL染色检测神经元凋亡情况。
与假手术组相比,其他三组的神经功能评分、脑含水量和ROS含量均显著升高(均P<0.05)。SAH + ATX组的神经功能评分、脑含水量和ROS含量均低于SAH组(均P<0.05)。与假手术组相比,其他三组白细胞介素(IL)-6、IL-17和肿瘤坏死因子α(TNF-α)表达增加,神经元凋亡增加,NOX2、GFAP和Bax表达增强;而IL-10表达降低,Bcl-2表达下降(均P<0.05)。与SAH组相比,SAH + ATX组IL-6、IL-17和TNF-α表达降低,NOX2、GFAP和Bax表达下降,神经元凋亡减少;而IL-10表达增加,Bcl-2表达增强(均P<0.05)。SAH组和SAH + 溶剂组之间的所有指标均无显著差异(均P>0.05)。
虾青素可减轻SAH小鼠的神经元损伤,抑制炎症反应,改善氧化应激。因此,虾青素是一种治疗SAH的方法。