›› 2010, Vol. 41 ›› Issue (1): 9-12.doi: 10.3969/j.issn.0529-1356.2010.01.002

• 论著 • 上一篇    下一篇

胡黄连苷Ⅱ对大鼠脑缺血再灌注损伤的干预作用

李震1;李琴1;郭云良1* ;秦丽华2;栾丽菊2   

  1. 1. 青岛大学医学院脑血管病研究所,青岛266003;2. 北京大学医学部解剖学系,北京100083
  • 收稿日期:2009-05-05 修回日期:2009-07-08 出版日期:2010-02-06
  • 通讯作者: 郭云良

Interference effect of picrosideⅡon cerebral ischemia reperfusion injury in rats

  1. 1. Institute of Cerebrovascular Diseases, Qingdao University Medical College, Qingdao 266003, China; 2. Department of Anatomy, Beijing University Medical College, Beijing100083, China
  • Received:2009-05-05 Revised:2009-07-08 Online:2010-02-06
  • Contact: GUO Yun-liang

关键词: 脑缺血, 再灌注损伤, 胡黄连苷Ⅱ, 原位缺口末端标记, 大鼠

Abstract: Objective To investigate the neuroprotective effects of picrodideⅡ on cerebral ischemic reperfusion injury in rats. Methods Intraluminal thread methods were applied to establish the left middle cerebral artery occlusion reperfusion models (MCAO/R) in rats. PicrodideⅡ (10mg/kg) and salvianic acid A sodium (10mg/kg) were injected from tail vein for treatment. The neurological behavioral function was evaluated with Bederson’s test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The structure of cells was observed with histopathology. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase midiated dUTP nick end labeling (TUNEL). Results The neurological behavioral malfunction appeared in all rats with MCAO/R. The infarction focus showed in the ischemic hemisphere following cerebral ischemia reperfusion injury. In the picrodideⅡ and salvianic acid A sodium treatment groups, the number of apoptosis positive cells decreased and the cerebral infarction volume reduced, while the neurological behavioral function was significantly improved than those in the model control group (EM>P/EM><0.05). The cerebral infarction volume in the picrodideⅡ group was smaller than that in the salvianic acid A sodium group (EM>P/EM><0.05).Conclusion PicrodideⅡ might reduce cerebral infarction volume and improve the neurological behavioral function through inhibit

Key words: Cerebral ischemia, Reperfusion injury, PicrodideⅡ, TUNEL, Rat

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