摘要
目的探讨PACAP对大鼠局灶性脑缺血-再灌注损伤后脑保护作用及保护机制。方法采用大脑中动脉线栓法建立局灶性脑缺血-再灌注模型,对36只大鼠随机分为假手术组、缺血-再灌注组和PACAP组,在大鼠脑缺血2h后进行12h、24h再灌注,比较光镜下细胞损伤变性程度,应用免疫组化法检测IL-1β的表达。结果PACAP组大鼠脑标本光镜下细胞损伤变性程度与缺血-再灌注组相比明显减轻;IL-1β灰度值PACAP组分别为120±5、114±4,与缺血-再灌注组178±4、162±6比较,有显著性差异(P<0.01)。结论PACAP能抑制大鼠局灶性脑缺血-再灌注时IL-1β的表达,可能是其脑保护作用之一。
Objective To explore the mechanism of PACAP neuroprotective function on focal cerebral ischemia-reperfusion injury in rats. Methods The model of focal cerebral ischemia-reperfusion injury was made by occluding middle cerebral artery （MCA） for 2h and reperfusing for 12h,24h. Thirty-six male Sprague-Dawley rats were randomized into Sham-operation group, ischemia-reperfusion group and PACAP group. Sections of every rat were processed with HE staining, immunohistochemistry staining. Results Compared to ischemia-reperfusion group, the injury degree of neuron greatly reduced. The section of PAC- AP group showed the number of injuried neuron and inflammatory cells less than that of ischemia-reperfusion group. The expressions of IL-1β in PACAP group were 120±5 and 114±4 . Compared with 178±4 and 162±6 in I/R group, there was significant difference（P 〈0. 01, P 〈0. 01）. Conclusion The administration of PACAP could decrease the expression of IL-1β after cerebral ischemia-reperfusion injury in rats. It is one of the mechanisms of neuroproteetive function.
出处
《中国实用神经疾病杂志》
2009年第7期21-23,共3页
Chinese Journal of Practical Nervous Diseases
