Relationship between hypoxia-inducible factor-1α expression and apoptosis in early brain injury models after subarachnoid hemorrhage
10.3760/cma.j.issn.1671-8925.2015.09.011
- VernacularTitle:HIF-1α与大鼠蛛网膜下腔出血后早期脑损伤的相关性研究
- Author:
Yuanfeng ZHANG
1
;
Jiandang ZHANG
;
Kunpeng WANG
;
Ruixun SUN
;
Sujie LIU
;
Dongbo ZHANG
;
Guanji ZHAO
Author Information
1. 473009,南阳市中心医院神经外科
- Keywords:
Subarachnoid hemorrhage;
Hypoxia-inducible factor-1α;
Brain injury;
Apoptosis
- From:
Chinese Journal of Neuromedicine
2015;14(9):918-922
- CountryChina
- Language:Chinese
-
Abstract:
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=1 1).SAH in the later four groups was induced by modified monofilament puncture method.The rats were killed by cervical dislocation.HIF-1α expression was assessed by immunofluorescence 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-1α positive cells were coincided with glial fibrillary acidic protein staining cells.A significant positive correlation was noted between HIF-1 α expression percentage and TUNEL positive rate following SAH (r=0.737,P=0.001).Conclusion HIF-1α high expression after SAH early promotes neuronal cell apoptosis,indicating HIF-1 a might participate in the pathological progression of early brain injury after SAH.
