摘要
目的探讨疏血通对脑缺血-再灌注后神经保护作用的机制,拟为临床应用提供理论依据。方法90只健康雄性SD大鼠,随机分为假手术组、缺血-再灌注组和疏血通治疗组,建立大脑中动脉闭塞模型。采用神经功能缺损评分对大鼠神经功能缺损程度进行评价,HE染色、TUNEL染色和免疫组织化学染色检测大鼠脑组织梗死灶体积、细胞凋亡及hsp70表达水平。结果经疏血通治疗后,大鼠神经功能缺损程度明显改善,除再灌注后6h,其余各时间点疏血通治疗组评分均优于缺血-再灌注组（P〈0.05）。疏血通治疗组大鼠梗死灶体积明显缩小（P〈0.01）。再灌注后6h,缺血半暗带区和海马区即可见凋亡细胞,分别于再灌注后48h和72h达峰值水平,疏血通治疗组表达高峰时间延迟,且各时间点凋亡细胞数目均少于缺血-再灌注组（P〈0.05）。再灌注后6h,缺血半暗带区和大脑皮质即可见少量hsp70表达阳性细胞,两组均于再灌注后24h达峰值水平,但疏血通治疗组各时间点hsp表达水平均高于缺血-再灌注组（P〈0.05）。结论疏血通通过上调脑组织hsp70表达水平,减轻脑缺血-再灌注损伤,从而使梗死灶体积缩小、神经功能改善。
Objective To explore the neuroprotection mechanism of shuxuetong after cerebral ischemia-reperfusion injury. Methods Ninty healthy Sprague-Dawley （SD） male rats were randomly divided into sham-operation group （n = 6）, ischemia-reperfusion group （n = 42） and shuxuetong treated group （n = 42）. Established middle cerebral artery occlusion （MCAO） model and observed the changes of infarction volume, apoptosis and hot-shock protein 70 （hsp 70） expression by HE staining, TUNEL staining and immunohistochemical staining, respectively. Neural functional deficit was assessed. Results The neural function in shuxuetong treated group was much better than that in ischemia-reperfusion group at every time points （P 〈 0.05, for all） except at 6 h after reperfusion （P 〉 0.05）. The infarction volume in shuxuetong treated group was obviously smaller than that in ischemia-reperfusion group （P 〈 0.01, for all）. Apoptosis cells were found in the ischemic semi-dark band area and hippocampus at 6 h after reperfusion in ischemia-reperfusion group and shuxuetong treated group, and achieved peak at 48 h and 72 h after reperfusion, respectively, but the amount of apoptosis cells in shuxuetong treated group was all less than that in ischemia-reperfusion group at every time points （P 〈 0.05, for all）. TUNEL-positive cells were more apparent in the perifocal tissue and particularly in the inner border regions immediately adjacent to the ischemic core. There were small amount of hsp70 positive cells in the ischemic semi-dark band area and cerebral cortex at 6 h after reperfusion in both groups. The expression achieved peak at 24 h after reperfusion in both groups, but hsp70 positive cells in shuxuetong treated group were more than those in ischemia-reperfusion group at every time points （P 〈 0.05, for all）. Conclusion It is suggested that shuxuetong can promote hsp70 expression, reduce cerebral ischemia-reperfusion injury and decrease infarction volume, and thus improve neural function.
出处
《中国现代神经疾病杂志》
CAS
2009年第2期168-172,共5页
Chinese Journal of Contemporary Neurology and Neurosurgery
