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中国临床药理学与治疗学 ›› 2015, Vol. 20 ›› Issue (6): 634-639.

• 基础研究 • 上一篇    下一篇

银杏内酯注射液抑制脑缺血再灌注模型大鼠内质网应激和自噬

兰新新1,曹磊2,王林晓3,丁建花3,范益3,胡刚3   

  1. 1. 南京医科大学
    2. 南京医科大学神经药理实验室
    3. 210029 南京医科大学药理学系
  • 收稿日期:2015-05-14 修回日期:2014-12-11 出版日期:2015-06-26 发布日期:2015-06-29
  • 通讯作者: 胡刚 E-mail:ghu@njmu.edu.cn
  • 基金资助:

    天然药物活性组分与药效国家重点实验室开放课题项目

Ginkgolides Injection Inhibits Endoplasmic Reticulum Stress and Attenuates Autophagy in Rat Brain induced by Cerebral Ischemia Reperfusion.

  • Received:2015-05-14 Revised:2014-12-11 Online:2015-06-26 Published:2015-06-29
  • Contact: Gang Hu E-mail:ghu@njmu.edu.cn

摘要: 【摘要】目的:探讨银杏内酯注射液(the Ginkgolides Injection, GIs)对大鼠脑缺血再灌注损伤的保护作用及其可能机制。方法:采用Longa法制备大鼠短暂性大脑中动脉阻塞(tMCAO)/再灌注损伤模型,于缺血再灌注1h后腹腔注射(ip, bid)不同剂量的GIs(1.25、2.5、5mg/kg),连续治疗3天并进行神经功能评分,干湿重法测定脑组织含水量,TTC染色法测定脑梗死体积;制备大鼠tMCAO模型,于再灌注1h给予GIs (2.5mg/kg),24h和72h 时取样,Western Blotting法检测缺血半影区内质网应激、自噬等相关蛋白表达。结果:GIs(2.5、5mg/kg)显著改善tMCAO模型大鼠神经运动功能障碍,减轻脑水肿,减小脑梗死体积;GIs显著抑制缺血再灌注损伤引起的大鼠缺血半影区内质网应激和自噬水平上升。结论:银杏内酯注射液通过降低内质网应激和自噬水平,减轻脑缺血再灌注损伤。

Abstract: 【ABSTRACT】Objective: To investigate the neuroprotective effects of the Ginkgolides Injection (GIs) against ischemic stroke-induced injury and further explore the possible mechanisms concerned. Methods: The modified method of Zea Longa was used to establish the transient middle cerebral artery occlusion (tMCAO) model in rats. GIs was injected intraperitoneally (ip, bid, 3d) to rats 1h after onset of reperfusion with different doses (1.25, 2.5 and 5mg/kg). The neurological deficits were assessed in each group after cerebral ischemia. Brain water content was measured by wet/dry weight method and Infarct volume was observed by TTC staining. Western Blot was used to evaluate the expression level of protein related to ER stress and autophagy in penumbra region of rats treated with GIs (2.5mg/kg) at 24h and 72h after reperfusion. Results: GIs (2.5 and 5mg/kg) treatment significantly reduced neurological deficits, water content, and cerebral infarct volume after stroke. GIs (2.5mg/kg) treatment protected against ischemia/reperfusion-induced ER stress and autophagy. Conclusions: GIs are neuroprotective against ischemic brain injury through the down regulation of ER stress and autophagy.