Protective effect of mitochondria-targeted antioxidant SS31 on early brain injury following subarachnoid hemorrhage in rats
10.11817/j.issn.1672-7347.2017.09.002
- VernacularTitle:线粒体靶向抗氧化剂SS31对大鼠蛛网膜下腔出血后早期脑损伤的保护作用
- Author:
Jian ZHOU
1
;
Zhengzheng LI
;
Zhenggang CHEN
;
Kun YANG
Author Information
1. 海南医学院第一附属医院神经外科
- Keywords:
SS31;
subarachnoid hemorrhage;
early brain injury;
oxidative stress;
apoptosis;
mitochondria
- From:
Journal of Central South University(Medical Sciences)
2017;42(9):1003-1009
- CountryChina
- Language:Chinese
-
Abstract:
Objective: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 SAHinduced 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 ofcytosolic 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.
