摘要
目的研究大鼠脑缺血再灌注损伤后Fas和FasI。蛋白的表达和丁笨酞保护作用的机制。方法线栓法制备大鼠大脑中动脉缺血再灌注模型,SD大鼠随机分为正常对照组、假手术组、缺血再灌注组和丁苯酞组;应用尼氏染色显示存活神经元,末端转移酶介导的缺口末端标记(TUNEI。)方法检测程序化死亡细胞;免疫组织化学法观察脑缺血再灌注后6h、1d、3d、7d四个时间点脑组织中Fas和FasI.蛋白的表达变化。结果丁苯酞组皮层存活神经元数量多于缺血再灌注组,TUNEI.阳性细胞数减少,丁苯酞组在再灌注后各时间点的Fas和FasL阳性细胞数较缺血再灌注组少,差异均有统计学意义。结论丁苯酞可能通过抑制Fas/FasL蛋白的表达,从而减少神经元凋亡,减轻缺血再灌注后脑组织的损伤。
Objective To investigate the expression of Fas and FasL proteins and the curative effects of dl--3--n--butylphthalide through the expression of the Fas and FasL proteins after cerebral ischemia-- reperfusion in adult male rats. Methods Ischemia insult was accomplished by using the intraluminal filament model of MCAO and rats were reperfused after 2h of artery occlusion. Healthy SD rats were divided into four groups.. Normal group, sham operation group, Ischemia reperfusion group, and dl--3--n--butylphthalide group. The dl--3--n--butylphthalide group was further divided into four sub- groups.. 6 hours, 1 day, 3 days, and 7 days after ischemia reperfusion injury. The surviving neurons, programmed cell death, and the expression of Fas and FasL proteins in cortex were dynamically detected using cystal violet stain, TUNEL and immunohistochemcial methods. Results The numbers of the survi- ving neurons in cortex of the dl--3--n--butylphthalide group were significantly higher than those of the ischemia reperfusion group. The number of TUNEL positive cells in the dl--3--n--butylphthalid group was notably smaller than those in ischemia reperfusion group. The numbers of Fas and FasL positive cells in the dl -- 3 -- n-- butylphthalide group were obviously less than those of isehemia reperfusion group. Conclusions The curative effects of dl--3--n--butylphthalide on rat cerebral ischemia--reperfu- sion injury might act via lowering the expression of Fas and FasL proteins therefore inhibiting cell apop- tosis and reduce neuronal death.
出处
《神经疾病与精神卫生》
2013年第1期50-53,共4页
Journal of Neuroscience and Mental Health
关键词
丁苯酞
脑缺血再灌注
FAS
FasI
凋亡
大鼠
D1-- 3 -- n-- butylphthalide
Cerebral ischemia-- reperfusion
Fas/FasL
Apoptosis
Rats