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

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

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 (transientmiddlecerebralar teryocclusion ,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dimethylsulfoxide ,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 (insituendlabeling ,ISEL)法研究脑组织细胞凋亡情况。结果 :(1)缺血 2h再灌注2 4h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 .5 3,预防组为0 .35± 0 .5 1,治疗组为 0 .6 2± 0 .5 2 ,防治组为 0 .2 5± 0 .4 6。 (2 )高倍视野下凋亡细胞数 :假手术组为1.88± 0 .2 5 ,I R组为 4 1.38± 3.85 ,DMSO组为38.13± 5 .6 9,预防组为 2 2 .88± 2 .70 ,治疗组为2 5 .6 3± 2 .93,防治组为 2 0 .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 .0 5 )。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。

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.