[Protective effect of mitochondria-targeted antioxidant SS31 on early brain injury following subarachnoid hemorrhage in rats].

To evaluate protective effects of SS31 on early brain injury (EBI) induced by subarachnoid hemorrhage (SAH) in rats. Methods: A total of 96 Sprague-Dawley rats were randomly divided into 4 groups: A sham group, an SAH group, an SAH+vehicle group (SAH+V), and an SAH+SS31 group. The SAH-induced prechiasmatic cistern rat model was established in this study. Neurological deficit scores were evaluated at 24 h after SAH. The SS31 (5 mg/kg) as well as equal volume of vehicle were administrated intraperitoneally at 2 h after SAH. The neurological scores, brain edema, blood-brain barrier (BBB) permeability, apoptosis, malondialdehyde (MDA), glutathione peroxidase (GPx) activity, superoride dismutase (SOD) activity, and the expression of cytosolic cytochrome c (Cyt C) and Bax were analyzed at 24 h after SAH. Results: Treatment with SS31 could significantly reduce MDA levels, and restored the activities of GPx and SOD in the cortex following SAH when compared with the SAH+V group. In addition, Bax SS31 trearment increased or decreased the levels of mitochondrial Cyt C or Bax, respectively. Moreover, SS31 treatment ameliorated brain edema and Evans blue dye extravasation, improved neurological deficits, and decreased neuronal apoptosis at 24 h after SAH. Conclusion: SS31 could alleviate EBI after SAH through its antioxidant property and ability in inhibition of neuronal apoptosis.目的：探讨SS31对蛛网膜下腔出血(subarachnoid hemorrhage，SAH)后早期脑损伤(early brain injury，EBI)的保护作用。方法：将96只大鼠随机分为假手术组(Sham)、SAH组、SAH+vehicle组(SAH+V)、SAH+SS31组。建立大鼠视交叉池SAH模型，术后2 h经腹腔注射SS31(5 mg/kg)或等体积的溶剂。在SAH后24 h，分析不同组间大鼠神经功能评分、脑水肿、伊文思蓝的渗出、细胞凋亡、丙二醛(malondialdehyde，MDA)、超氧化物歧化酶(superoxide dismutase，SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase，GPx)、细胞色素(cytochrome c，Cyt C)及Bax表达水平的差异。 结果：与SAH+V组比较，SS31治疗能显著降低SAH 后大鼠脑组织中MDA 水平，提高GPx和SOD 活性，上调线粒体Cyt C表达水平，降低Bax表达水平，脑水肿和伊文思蓝的渗出减轻，改善大鼠神经功能缺损，减少神经元凋亡。结论：SS31可减轻SAH后EBI，其机制可能与抗氧化应激和抑制神经元凋亡有关。.