中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (10): 900-908.doi: 10.3969/j.issn.1673-5374.2013.10.004

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

美满霉素对缺血再灌注脑损伤的影响

  

  • 收稿日期:2012-07-03 修回日期:2013-01-21 出版日期:2013-04-05 发布日期:2013-04-05

Effect of minocycline on cerebral ischemia- reperfusion injury

Yuanyin Zheng1, 2, Lijuan Xu1, Jinbao Yin3, Zhichao Zhong1, Hongling Fan1, Xi Li1, Quanzhong Chang1   

  1. 1 Department of Physiology, Zhuhai Campus of Zunyi Medical College, Zhuhai 519041, Guangdong Province, China
    2 Department of Pathology, Mindong Hospital of Fujian Medical University, Fuan 355000, Fujian Province, China
    3 Department of Pathology, Guangdong Medical College, Dongguan 523808, Guangdong Province, China
  • Received:2012-07-03 Revised:2013-01-21 Online:2013-04-05 Published:2013-04-05
  • Contact: Quanzhong Chang, Ph.D., Professor, Department of Physiology, Zhuhai Campus of Zunyi Medical College, Zhuhai 519041, Guangdong Province, China, cqzchang@tom.com
  • About author:Yuanyin Zheng★, Master.

PDF

705

摘要：

鉴于四环素衍生物抗生素美满霉素能够穿越血脑屏障，进入中枢神经系统。实验以线拴法建立脑缺血再灌注大鼠模型，腹腔注射美满霉素（22.5mg/kg，首次45mg/kg），间隔12h一次，以验证其作用和机制。结果显示，美满霉素治疗后，缺血再灌注大鼠脑梗死体积明显减小，海马CA1区存活神经元数量增加，凋亡细胞数量减少，且海马CA1区Caspase-3和聚腺苷酸二磷酸核糖转移酶1表达减少，而水迷宫实验的逃避潜伏期明显缩短。结果提示美满霉素对缺血再灌注损伤具有一定的保护作用，其机制可能与抑制caspase-3和聚腺苷酸二磷酸核糖转移酶1的表达有关。

关键词: 神经再生, 脑损伤, 美满霉素, 脑缺血再灌注, 海马, 聚腺苷酸二磷酸核糖转移酶1, Caspase-3, 细胞凋亡, 基金资助文章

Abstract:

Minocylcine, a tetracycline derivate, has been shown to cross the blood-brain barrier and enter the central nervous system. In this study, cerebral ischemia-reperfusion injury models were established using the suture method, and minocycline was immediately injected intraperitoneally after cerebral ischemia-reperfusion (22.5 mg/kg, initially 45 mg/kg) at a 12-hour interval. Results showed that after minocycline treatment, the volume of cerebral infarction was significantly reduced, the number of surviving cell in the hippocampal CA1 region increased, the number of apoptotic cells decreased, the expression of caspase-3 and poly(adenosine diphosphate-ribose) polymerase-1 protein was down-regulated, and the escape latency in the water maze test was significantly shortened compared with the ischemia-reperfusion group. Our experimental findings indicate that minocycline can protect against neuronal injury induced by focal ischemia-reperfusion, which may be mediated by the inhibition of caspase-3 and poly(adenosine diphosphate-ribose) polymerase-1 protein expression.

Key words: neural regeneration, brain injury, minocycline, cerebral ischemia-reperfusion, hippocampus, poly (adenosine diphosphate-ribose) polymerase-1, caspase-3, apoptosis, grants-supported paper, neuroregeneration