Progesterone inhibits ischemic brain injury in a rat model of permanent middle cerebral artery occlusion.
Progesterone inhibits ischemic brain injury in a rat model of permanent middle cerebral artery occlusion.
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发表时间：
2007
影响因子：
2.8
通讯作者：
I. Sayeed;Bushra Wali;D. Stein
中科院分区：
文献类型：
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作者：
I. Sayeed;Bushra Wali;D. Stein
目的以往的研究表明，孕酮(Prog)对多种类型的脑损伤有显著的保护作用。由于大多数人类中风是由永久性脑动脉闭塞引起的，我们在永久性MCAO(PMCAO)模型中评估了Prog对脑梗塞和行为障碍的神经保护作用。方法将硅胶涂层尼龙纤维植入右侧颈内动脉制作大鼠大脑中动脉闭塞模型。结扎后10min用激光多普勒血流仪监测脑血流量。分别于结扎后1h给予Prog(8 mg/kg)或赋形剂(2-羟丙基-β-环糊精)，再于结扎后6、24、48h皮下注射。分别于72 h测量脑梗塞体积(皮质、皮质下和总体积)，24、48和72 h进行功能恢复。结果PROG治疗后，染色切片显示，与载体注射对照组相比，皮质、尾壳核和大脑半球梗死体积(对侧结构的百分比)显著减少。此外，PROG治疗减少了加速旋转棒装置的功能缺陷。结论在大鼠局灶性脑缺血模型上证实了PROG的神经保护作用。
PURPOSE Previous studies suggest that progesterone (PROG) has a substantial protective effect against several types of brain injury. Since most cases of human stroke are caused by permanent occlusion of cerebral arteries, we assessed the neuroprotective effects of PROG on cerebral infarction and behavioral deficits in a permanent MCAO (pMCAO) model. METHODS pMCAO was produced by surgical insertion of a silicone-coated nylon filament into the right internal carotid artery. Laser-Doppler flowmetry was used to monitor cerebral blood flow for 10 min post-occlusion. PROG (8 mg/kg) or vehicle (2-hydroxypropyl-beta-cyclodextrin) was administered intraperitoneally at 1 h post-occlusion followed by subcutaneous injections at 6, 24 and 48 h post-occlusion. Measurements of infarct volumes (cortical, subcortical and total) were performed at 72 h and functional recovery, assessed by rotarod test, were performed 24, 48, and 72 h after pMCAO. RESULTS Following PROG treatment, stained sections revealed a significant reduction in cortical, caudate-putamen and hemispheric infarct volumes (% contralateral structure) compared to vehicle-injected controls. In addition, PROG treatment reduced functional deficits on the accelerating rotarod apparatus. CONCLUSION We demonstrated and confirmed the neuroprotective effect of PROG using a permanent model of focal brain ischemia in rats.