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

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。

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

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.