虾青素对兔蛛网膜下腔出血后的保护作用研究

Protection of astaxanthin on subarachnoid hemorrhage in rabbits

目的研究虾青素对兔蛛网膜下腔出血(SAH)的保护作用。方法成年雄性新西兰大白兔15只,随机分为对照组(control)、SAH加安慰剂组(SAH+vehicle)和虾青素治疗组(SAH+ATX)。通过建立兔枕大池注血SAH模型,于手术后24 h记录神经功能评分,并应用末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)、以及分光光度比色法分别检测脑组织神经细胞病理学改变,和脑组织丙二醛(MDA)、谷胱甘肽(GSH)及超氧化物歧化酶(SOD)的变化。结果与对照组相比,SAH后兔神经功能损伤评分加重,脑组织中TUNEL凋亡阳性细胞数也显著增多;应用虾青素干预以后,兔神经功能改善,脑组织TUNEL凋亡阳性细胞明显减少。同时,虾青素能够降低SAH后兔脑组织中MDA水平,并提高GSH含量和SOD活性。结论虾青素对SAH后早期脑损伤(EBI)具有保护作用,其作用机制可能与其抗氧化性有关。

Objective The protection of astaxanthin（ ATX） on subarachnoid hemorrhage（ SAH） in rabbits is studied. Methods A total of 15 New Zealand male rabbits were randomly divided into three groups： control group,SAH ＋ vehicle group and SAH ＋ ATX group. The cisterna magna SAH rabbit model was established in this experiment. Neurological deficit scores were evaluated at 24 h after surgery. The changes in histopathology and the variation of malondialdehyde（ MDA）,glutathione（ GSH）,and superoxide dismutase（ SOD） in the brain cortex were evaluated by terminal deoxynucleotidyl transferase-mediated deoxyufidine triphosphate nick-end labeling（ TUNEL）staining and spectrophotometric method,respectively. Results Compared with control group,the clinical behavior function impairment caused by SAH deteriorated in SAH ＋ vehicle group. In addition,the apoptotic cells were increased in the cerebral cortex followed SAH. After ATX administration,the neurological dysfunction and neural cell apoptosis were ameliorated after SAH. Meanwhile,ATX could reduce MDA levels,and restore the GSH contents and SOD activity in the brain cortex following SAH in rabbits. Conclusion ATX can alleviate EBI after SAH by its antioxidant property.