引用本文:高 政 1,姜丽杰 2 ,邢芸芸 3 ,王旭刚 1.预防性应用盐酸氟桂利嗪对高血糖SD大鼠局部脑缺血再灌注模型ICAM-1表达的影响[J].大连医科大学学报,2012,34(4):339-342.
【打印本页】   【HTML】   【下载PDF全文】   查看/发表评论  【EndNote】   【RefMan】   【BibTex】
←前一篇|后一篇→ 过刊浏览    高级检索
本文已被:浏览 次   下载 本文二维码信息
码上扫一扫!
分享到: 微信 更多
预防性应用盐酸氟桂利嗪对高血糖SD大鼠局部脑缺血再灌注模型ICAM-1表达的影响
高 政 1,姜丽杰 2 ,邢芸芸 3 ,王旭刚 11,2,3
1.大连医科大学 附属第二医院北院 神经内科,辽宁 大连 116031;2.大连市第三人民医院 神经内科,辽宁 大连 116031;3.沈阳市第四人民医院 心内科,辽宁 沈阳 110031
摘要:
[目的] 探讨预防性应用盐酸氟桂利嗪对高血糖条件下SD大鼠局灶性脑缺血再灌注损伤是否有保护作用及其可能机制。 [方法] 雄性健康SD大鼠36只,建立高血糖模型后随机分为两组:高血糖组(n=18)与盐酸氟桂利嗪+高血糖组(简称氟桂利嗪组,n=18),各组按脑缺血90 min再灌注3 h(n=6)、6 h(n=6)、24 h(n=6)分为3个亚组。比较氟桂利嗪组与高血糖组各再灌注时间点脑组织病理形态改变及ICAM-1表达的动态变化。 [结果] 脑组织病理形态观察:氟桂利嗪组随着再灌注时间的延长,脑组织受损程度逐渐加重,但与高血糖组各时间点比较,变性、坏死的神经元较少,组织间水肿较轻。ICAM-1表达:氟桂利嗪组于再灌注3 h可见ICAM-1阳性表达,24 h内逐渐增高(P<0.05)。氟桂利嗪组与高血糖组比较各时间点缺血区ICAM-1表达均减少(P<0.01)。 [结论] 预防性应用盐酸氟桂利嗪能减轻高血糖条件下的局灶性脑缺血再灌注损伤。
关键词:  盐酸氟桂利嗪  高血糖  脑缺血再灌注  细胞间粘附分子-1
DOI:10.11724/jdmu.2012.04.06
分类号:
基金项目:
Effect of pretreatment by flunarizine hydrochlorid on focal cerebral ischemia reperfusion damage and the expression of ICAM-1 in rats with hyperglycemia
GAO Zheng 1,JIANG Li-jie 2,XING Yun-yun 3,WANG Xu-gang 11,2,3
1.Department of Neurology,The North Hospital of Dalian Medical University No.2 Affiliated Hospital, Dalian 116031,China;2. Department of Neurology, Third People’s Hospital of Dalian, Dalian 116031, China;3. Department of Cardiology, Fourth People’s Hospital of Shenyang, Shenyang 110031, China
Abstract:
[Objective] To investigate whether pretreatment with flunarizine hydrochlorid could relieve the injury of local cerebral ischemia-reperfusion in rats with hyperglycemia. [Method] Thirty six healthy male SD rats (weight from 180 g to 220 g) were randomly divided into 2 groups: hyperglycemia group (n=18) and flunarizine +hyperglycemia group(flunarizine group n=18). The rats in each group were divided into 3 subgroups according to reperfusion 3 h (n=6), 6 h (n=6) and 24 h (n=6) after ischemia for 90 minutes. The differences of cerebral pathological changes and the expressions of ICAM-1 among these groups. [Result] Compared with hyperglycemia group, the number of degenerative and necrosis neurons were less and tissue edema became was weaker. In the flunarizine group, the expression of ICAM-1 can be seen at 3 hours from reperfusion, and increase in 24 hours from reperfusion, P<0.05. Compared with hyperglycemia group at every reperfusion time: ICAM-1 expressions were decreased in flunarizine group, P<0.01. [Conclusion] The pretreatment of flunarizine hydrochlorid could decrease the expression of ICAM-1 and the focal ischemia-reperfusion damage of the ras with hyperglycemia.
Key words:  flunarizine hydrochlorid  hyperglycemia  ischemia reperfusion  ICAM-1