丁苯酞对大鼠脑缺血再灌注损伤后HSP10表达的影响

Effects of dl-3-butylphthalide on the expression of HSP10 in the rat brain tissues following cerebral ischemiareperfusion injury

目的研究丁苯酞干预对大鼠脑缺血再灌注损伤后不同时点脑组织中热休克蛋白10(HSP10)表达的影响,并探讨丁苯酞对缺血性脑血管病保护作用的机制。方法采用夹闭双侧颈总动脉的方法制作大鼠前脑缺血再灌注模型;H&E染色和NSE免疫组化染色神经元,观察脑组织的形态变化和记数各组神经元数目;免疫组织化学检测对照组、缺血再灌注组及丁苯酞干预组大鼠脑组织HSP10的表达水平变化。结果脑缺血再灌注后丁苯酞干预组及缺血再灌注组HSP10表达水平于再灌注后6h开始上调,3d达到高峰,丁苯酞干预组各时间点HSP10阳性表达指数均高于缺血再灌注组,丁苯酞干预组脑组织的损伤程度明显轻于脑缺血再灌注组(P<0.05)。结论丁苯酞可能通过上调大鼠缺血再灌注损伤后脑组织HSP10的表达,从而抑制前脑缺血再灌注损伤后细胞凋亡,减少神经元死亡,减轻缺血再灌注后脑组织的损伤。

Objective To investigate the effect of dl-3-butylphthalide（NBP） on the expression of heat shock protein 10 （HSP10） in the rat brain tissues following cerebral ischemia-reperfusion（IR） injury and to study the molecular mechanism of the curative effect of NBP. Methods A cerebral IR model in the rat was es- tablished by clamping both common carotids. H＆E staining and immunohistochemical detection of NSE ex- pression in neurons were used to count the number of neurons and characteristics of tissue injury in each group under the light microscope. The expression of HSP10 in brain tissue was detected by immunohistochemistry technique. Results In NBP intervention group and IR group, expression of HSP10 was significantly increased at 6h and came to the highest level at the 3rd day following IR. At four different time points, the positive ex- pression of HSP10 in NBP group was significantly higher than that in IR group and the degree of brain damage in the NBP intervention group was significantly milder than that in IR group （P〈0.05）. Conclusions The NBP can reduce neuronal damage in the rat brain tissue following cerebral IR, which may be associated with increased expression of HSP10.