摘要
目的探讨大脑皮层低氧诱导因子-1α（HIF-1α）与蛛网膜下腔出血（sAH）后早期脑损伤的相关性。方法选取55只成年健康雄性Sprague．Dawley大鼠，按随机数字表法分为假手术组、SAH6h组、SAH12h组、SAH24h组及SAH72h组（n=11），其中后4组通过改良的血管内穿刺法建立SAH模型并在相应时间点采取颈椎脱臼法处死。应用TUNEL法检测各组大鼠神经元细胞凋亡情况．应用免疫荧光染色检测HIF-1α的表达水平，应用免疫荧光双标染色检测表达HIF-1α的细胞类型：应用Pearson相关法分析TUNEL阳性率与HIF-1α表达阳性率之间的相关性。结果与假手术组相比．各SAH组TUNEL阳性率和HIF-1α表达阳性率均显著升高．差异均有统计学意义fP〈0．05）。免疫荧光双标染色显示神经元特异性核蛋白（NeuN）染色阳性细胞与多数HIF-1α表达阳性细胞重合，胶质纤维酸性蛋白（GFAP）染色阳性细胞与少数HIF-1α表达阳性细胞重合。同时．部分TUNEL染色阳性细胞与HIF-1α表达阳性细胞重合，Pearson相关分析显示HIF-1α表达阳性率与TUNEL阳性率呈正相关关系（r=0．737，P=0．001）。结论在SAH后早期脑损伤的病理生理过程中．HIF-1α高表达加剧了神经元的凋亡。
Objective To explore the relationship between hypoxia-inducible factor-1α （HIF-1α） expression and apoptosis in early brain injury models after subarachnoid hemorrhage （SAH）. Methods Fifty-five adult male Sprague-Dawley rats were randomly assigned to five groups： sham-operated group, SAH 6 h, SAH 12 h, SAH 24 h and SAH 72 h groups （n=11）. SAH in the later four groups was induced by modified monofilament puncture method. The rats were killed by cervical dislocation. HIF-lct expression was assessed by immunoftuorescence staining. TUNEL was adopted to detect brain apoptotic cells. Immunofluorescence double staining was used to identify cell types with positive HIF-1α expression. Pearson correlation analysis was employed to analyze the relationship between HIF-1 expression percentage and TUNEL positive rate. Results As compared with those in the sham-operated group, the HIF-1 expression percentage and TUNEL positive rate in the four SAH groups was significantly higher （P〈0.05）. Immunofluorescence double staining showed that neuron-specific nuclear protein staining cells were coincided with most HIF-1 positive cells, while only a few HIF-lct positive cells were coincided with glial fibrillary acidic protein staining cells. A significant positive correlation was noted between HIF-1α expression percentage and TUNEL positive rate following SAH （r=0.737, P=0.001）. Conclusion HIF-lct high expression after SAH early promotes neuronal cell apoptosis, indicating HIF-1α might participate in the pathological progression of early brain injury after SAH.
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2015年第9期918-922,共5页
Chinese Journal of Neuromedicine
