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目的:研究补阳还五汤抗全脑缺血后再灌注损伤的分子机制。方法 :将66只SD大鼠随机分为3组,即正常组、模型组和药物组(补阳还五汤预干预),模型组和药物组再分别设置2、24 h 2个观察时间点。连续给药5 d后,采用改良的Pulsinelli四血管闭塞法复制全脑缺血大鼠模型,再灌后2、24 h采用免疫组化法检测各组大鼠皮质神经细胞NMDA受体(N-methyl-D-aspartic acid receptor)亚单位NR1的表达水平。结果 :与正常组比较,模型组2、24 h 2个不同时间点,NR1的表达水平显著升高(P<0.05);与模型组比较,药物组再灌注后2、24 h 2个不同时间点,NR1表达水平显著降低(P<0.01)。结论 :补阳还五汤预干预对全脑缺血再灌注模型大鼠大脑皮层神经元NR1表达水平的增高有调低作用。
Objective: To study the molecular mechanism of Buyang Huanwu decoction on reperfusion injury after global cerebral ischemia. Methods: Sixty-six Sprague-Dawley rats were randomly divided into three groups: normal group, model group and drug group (BYHWD pre-intervention). In model group and drug group, . After continuous administration for 5 days, the model of global cerebral ischemia was established by modified Pulsinelli four-vessel occlusion method. The expression of NMDA receptor (N-methyl-D-aspartate) in rat cortical neurons was detected by immunohistochemistry at 2, methyl-D-aspartic acid receptor subunit NR1 expression levels. Results: Compared with the normal group, the expression level of NR1 in the model group was significantly increased at 2 and 24 h (P <0.05) at 2 different time points. Compared with the model group, Point, NR1 expression was significantly lower (P <0.01). Conclusion: Pretreatment with Buyang Huanwu decoction can reduce the expression of NR1 in cerebral cortex neurons of rats with global cerebral ischemia and reperfusion.