摘要
目的：检测高血脂对脑缺血再灌注损伤后缺血侧大脑皮质p38丝裂原活化蛋白激酶（p38MAPK）表达的影响。方法：喂食高脂饲料建立高血脂动物模型，随后线栓法建立脑缺血再灌注模型。Zea-Longa神经行为学评分法记录大鼠神经行为改变，TTC染色检测脑梗死灶体积，免疫组织化学及免疫印迹检测大脑皮质p38MAPK表达水平。结果：高血脂脑缺血再灌注后神经行为损伤加重，且梗死灶体积较单纯脑缺血再灌注明显扩大。与假手术组比较，单纯脑缺血再灌注组和高血脂脑缺血再灌注组大脑皮质p38MAPK表达明显增加，再灌注2h时其表达量即开始增高，再灌注24h时达高峰，而后又降低。相同再灌注时间点，与单纯脑缺血再灌注组比较，高血脂脑缺血再灌注组p38MAPK表达增高。结论：高血脂脑缺血再灌注损伤中，高血脂可上调大脑皮质p38MAPK表达，促进细胞凋亡的发生及加重炎症反应，进而加重缺血再灌注损伤。
Objective： To explore the effect of hyperlipemia on the expression of p38MAPK in the cerebral cortex after cerebral ischemia-reperfusion injury in rats. Methods： The hyperlipemia model rats were given homemade high-fat diet. The focal cerebral ischemia-repeffusion model was established with thread embolism of the middle eerebral artery. The neurobehavioral changes of rats were observed using neurological behavioral evaluation. TTC staining was employed to assess the cerebral infarct volume. Immunohistochemistry and Western blotting were used to examine the expression of p38MAPK in the cerebral corte=~ ResMts： Compared with sham-operation group, the expression of p38MAPK in the cerebral cortex increased in the cerebral ischemia-reperfusion group and hyperlipemia with cerebral ischemia-reperfusion group, began to increase at reperfusion 2 h, reached the top at reperfusion 24 h and then decreased. Compared with the cerebral ischemia-reperfusion group, at the same reperfusion point, p38MAPK expression increased significantly in the hyperlipemia with cerebral isehemia-reperfusion group. Conclusion; Hyperlipemia can increase the expression of pg8MAPK in the cerebral cortex with ischemia-reperfusion injury, which aggravates cerebral isehemia-reperfusion injury by promoting apoptosis and inflammatory reaction.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2016年第6期698-701,F0003,共5页
Chinese Journal of Anatomy
基金
山西省高校科技研究开发项目(200613049)
关键词
高血脂
脑缺血再灌注
P38丝裂原活化蛋白激酶
大脑皮质
大鼠
hyperlipemia
cerebral ischemia-reperfusion
p38 mitogen activated protein kinase
cerebral cortex
rat
