Treatment with ginseng total saponins reduces the secondary brain injury in rat after cortical impact

被引:26
作者
Xia, Lei [1 ,2 ]
Jiang, Zheng-Lin [1 ]
Wang, Guo-Hua [1 ]
Hu, Bao-Yin [1 ]
Ke, Kai-Fu [3 ]
机构
[1] Nantong Univ, Dept Neuropharmacol, Inst Naut Med, Nantong 226001, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Neurol, Huaian Peoples Hosp 1, Huaian, Peoples R China
[3] Nantong Univ, Dept Neurol, Affiliated Hosp, Nantong 226001, Jiangsu, Peoples R China
关键词
ginseng total saponins; traumatic brain injury; oxidative stress; nitrative stress; inflammatory response; neuronal apoptosis; SUPPRESSING OXIDATIVE STRESS; NF-KAPPA-B; PANAX-GINSENG; RED GINSENG; HEAD-INJURY; PC12; CELLS; HIPPOCAMPAL-NEURONS; MOTOR-PERFORMANCE; INDUCED APOPTOSIS; GINSENOSIDES;
D O I
10.1002/jnr.22811
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The present study was designed to investigate the neuroprotective effect of ginseng total saponins (GTSs) and its underlying mechanisms in a rat model of traumatic brain injury (TBI). Rats were injected with GTSs (20 mg/kg, i.p.) or vehicle for 14 days after TBI. Neurological functions were determined using beam balance and prehensile traction tests at 114 days after trauma. Brain samples were extracted at 1 day after trauma for determination of water content, Nissl staining, enzyme-linked immunosorbent assay, immunohistochemistry, terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end labeling, and measurement of oxidative stress variables and inflammatory cytokines. Moreover, the dose response of the neuroprotective effect and time window of the efficacy of GTSs were also determined. We found that treatment of GTSs 1) improved the neurological function with an effective dosage of 580 mg/kg and an efficacy time window of 36 hr after TBI; 2) reduced brain water content and neuronal loss in the hippocampal CA3 area; 3) increased the activity of superoxide dismutase and decreased the activity of nitric oxide synthase and the amount of malondialdehyde and nitric oxide; 4) down-regulated interleukin-1 beta, interleukin-6, and tumor necrosis factor-a and upregulated interleukin-10 in the cortical area surrounding the injured core; and 5) inhibited the apoptotic cell death and expression of caspase-3 and bax and raised the expression of bcl-2. These findings suggest that administration of GTSs after TBI could reduce the secondary injury through inhibiting oxidative and nitrative stress, attenuating inflammatory response, and reducing apoptotic cell death. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:1424 / 1436
页数:13
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