http://jcps.bjmu.edu.cn

中国药学(英文版) ›› 2017, Vol. 26 ›› Issue (9): 684-691.DOI: 10.5246/jcps.2017.09.077

• 【研究论文】 • 上一篇    下一篇

薯蓣皂苷通过降低胶质细胞活化及维持SOD水平减轻脑卒中小鼠的神经损伤

尹成, 王杰, 徐沛, 颜丙春*   

  1. 江苏省中西医结合老年病防治重点实验室, 江苏 扬州 225001
  • 收稿日期:2017-05-27 修回日期:2017-07-13 出版日期:2017-09-30 发布日期:2017-08-25
  • 通讯作者: Tel.: +86-514-87992215, E-mail: bcyan@yzu.edu.cn
  • 基金资助:

    The National Natural Science Foundation of China (Grant No. 81401005), the Natural Science Foundation of Jiangsu Province of China (Grant No. BK20140494), and the College Students’ Practice Innovation Training Program Projects of Jiangsu Province (Grant No. 201611117094X).

Neuroprotective effect of dioscin on cerebral ischemia/reperfusion mice by reducing glial cell activation and maintaining the levels of SODs

Cheng Yin, Jie Wang, Pei Xu, Bingchun Yan*   

  1. Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University, Yangzhou225001, China
  • Received:2017-05-27 Revised:2017-07-13 Online:2017-09-30 Published:2017-08-25
  • Contact: Tel.: +86-514-87992215, E-mail: bcyan@yzu.edu.cn
  • Supported by:

    The National Natural Science Foundation of China (Grant No. 81401005), the Natural Science Foundation of Jiangsu Province of China (Grant No. BK20140494), and the College Students’ Practice Innovation Training Program Projects of Jiangsu Province (Grant No. 201611117094X).

摘要:

本实验主要是探究天然甾体皂苷-薯蓣皂苷对小鼠大脑中动脉阻断术后引起的局灶性脑缺血的神经保护作用及其相关作用机制。在本实验中, 我们发现薯蓣皂苷(1.5 mg/kg, 侧脑室注射)术前30 min给药后明显减少小鼠脑梗死体积和神经损伤症状, 同时脑梗死区神经细胞(神经元细胞、胶质细胞)的死亡及海马区神经胶质细胞的活化也显著减少; 另外, 1.5 mg/kg薯蓣皂苷干预明显提高脑梗死区SODs的表达。这些结果表明薯蓣皂苷通过抑制胶质细胞活化及提高SODs的表达对脑缺血再灌注小鼠发挥神经保护作用。

关键词: 薯蓣皂苷, 胶质细胞活化, 抗氧化, 神经保护, 脑缺血再灌注

Abstract:

In the present study, we aimed to explore the neuroprotective effect of dioscin, a natural steroid saponin, on transient focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) in mice and its related mechanism. We observed that dioscin (1.5 mg/kg, intracerebroventricular injection 30 min before MCAO) dramatically reduced the cerebral infarct volume, leading to improved neurological symptoms and reduced death of neuron, astrocytes and microglia in the infarct region. The gliosis and the reduced expressions of SOD1 and SOD2 by MCAO in the hippocampal CA1 region were significantly elevated by 1.5 mg/kg dioscin administration. These findings suggested that pretreatment of dioscin had a neuroprotective effect on mice transient focal cerebral ischemia via inhibiting the gliosis and elevating the SOD levels.

Key words: Dioscin, Gliosis, Antioxidant, Neuroprotection, Cerebral ischemia/reperfusion

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