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中国临床药理学与治疗学 ›› 2004, Vol. 9 ›› Issue (9): 1045-1049.

• 研究原著 • 上一篇    下一篇

黄体酮防治大鼠缺血再灌注脑损伤中神经功能缺失及细胞凋亡

李超, 卢娜1, 李东亮1, 张剑凯2   

  1. 新乡医学院第三附属医院眼科,1生理学教研室, 新乡453003, 河南;
    2湛江医学院解剖学教研室, 湛江524000, 广东
  • 收稿日期:2004-06-12 修回日期:2004-07-20 出版日期:2004-09-26 发布日期:2020-11-23
  • 通讯作者: 李超, 男, 硕士, 讲师, 主治医师, 研究方向:神经缺血再灌注损伤与防治。Tel:0373-5289582 E-mail:lichao1973 @etang. com
  • 基金资助:
    河南省教育厅资助项目(№20013100005)

Effects of progesterone on apoptosis and neuroprotective in rats during focal cerebral ischemia/reperfusion injury

LI Chao, DONG Liang-Li1, LU-Na1, ZHANG Jian-Kai2   

  1. Department of Ophthalmology, the Third Affiliated Hospital,1Department of Physiology, Xingxiang Medical College, Xingxiang 453003, Henan, China;
    2Department of anatomy, Zhanjiang Medical College, Zhanjiang 524000, Guangdong,China
  • Received:2004-06-12 Revised:2004-07-20 Online:2004-09-26 Published:2020-11-23

摘要: 目的: 探讨黄体酮(progesterone, PROG) 对脑缺血再灌注损伤的保护机制。方法: 采用SD 大鼠局灶性脑缺血再灌注模型(transient middle cerebral artery occlusion,MCAO) 。将大鼠随机分为6 组:假手术组、ischmia/reperfusion (I/R) 组、溶剂(二甲基亚砜dimethyl sulfoxide, DMSO) 对照组、PROG 预防组、PROG 治疗组、PROG 预防并治疗组, 对各组动物脑缺血/再灌注后神经功能缺陷进行计分, 并应用细胞死亡原位末端标记(insitu end labeling, ISEL) 法研究脑组织细胞凋亡情况。结果: (1) 缺血2 h 再灌注24 h 后神经功能缺陷计分:假手术组为0 分, I R 组为1. 38±0. 92, DMSO 组为1. 0±0. 53, 预防组为0. 35±0. 51, 治疗组为0. 62±0. 52, 防治组为0. 25±0. 46 。(2) 高倍视野下凋亡细胞数:假手术组为1. 88±0. 25, I R 组为41. 38±3. 85, DMSO 组为38. 13±5. 69, 预防组为22. 88±2. 70, 治疗组为25. 63±2. 93, 防治组为20. 88±2. 30 。以上指标各药物处理组(预防组、治疗组及防治组) 与I R 组、DMSO 对照组之间差异具有统计学意义(P<0. 05) 。结论: PROG 可减少局灶性缺血再灌注脑损伤动物模型神经功能缺失的发生, 减轻局灶性缺血再灌流脑损伤, 减少大鼠缺血再灌注后脑细胞凋亡。

关键词: 黄体酮, 脑缺血, 再灌注损伤, 神经功能缺陷, 凋亡

Abstract: AIM: To study the effects of neuroprotective and molecular mechanism of progesterone on ischemia reperfusion injury.METHODS: The rats with transient middle cerebral artery occlusion (MACO) were treated by Zea-Longa for 2 h and reperfused for 24 h. 48 male rats were divided into 6 group randomly. There were the sham group, ischmia/reperfusion (I/R), dimethl sulfoxide (DMSO), and pretreatment, posttreatment, pre +posttreament with PROG. The score of neurological deficit was measured by Zea-Longa method and insitu end labeling (ISEL) was used to investigate apoptosis in the brain tissues.RESULTS: The score of neurological deficit was 0 in the sham operation after reperfusion 24 h, 1. 38±0. 92 in the I/R group, 1. 0±0. 53 in the DMSO group, 0. 35±0. 51 in the pretreatment group, 0. 62±0. 52 in the posttreatment group, and 0. 25±0. 46 in the pre +posttreament group. The number of apoptosic cells was 1. 88±0. 25 in the sham group, 41. 38±3. 85 in the I/R group, 38. 13±5. 69 in the DMSO group, 22. 88±2. 70 in the pretreatment group, 25. 63±2. 93 in the posttreatment group, and 20. 88±2. 30 in the pre + posttreament group. There were significant differences in pretreament, posttreament, pre +posttreament and control groups(I/R or DMSO) (P<0. 05).CONCLUSION: PROG may protect the focal ischemia brain on reperfusion injury and reduce the expression of apoptosis and the neurological deficit.

Key words: progesterone, ischemia, reperfusion injury, neurological defici, apoptosis

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