论文部分内容阅读
目的 研究达纳康在大鼠局灶性脑缺血再灌注损伤中的脑保护作用及其分子机制。方法 采用线栓法建立大鼠大脑中动脉 ( MCAO)缺血 1h再灌注 2 4 h模型 ,18只雄性大鼠随机分为假手术组、生理盐水对照组和达纳康治疗组 ,每组 6只。采用 Zea- L onga评分法观察神经功能缺损程度 ,采用免疫组织化学方法、TUNEL 法分别观察各组 P53蛋白表达和细胞凋亡。结果 假手术组神经功能缺失评分为 0分 ,高倍视野下无 P53蛋白染色阳性细胞及凋亡细胞 ;达纳康治疗组神经功能缺失评分 ( 0 .4 8± 0 .3 7分 )、P53蛋白染色阳性细胞数 ( 5 .16± 1.84个 /高倍视野 )、凋亡细胞数 ( 4 .18± 1.2 1个 /高倍视野 )均较生理盐水对照组 ( 2 .76± 0 .82分、10 .4 3± 1.5 6个 /高倍视野、8.16± 1.5 0个 /高倍视野 )显著减少 ( P<0 .0 1)。结论 达纳康可明显减轻局灶性脑缺血再灌注损伤 ,其抑制神经细胞P53蛋白的表达 ,进而抑制细胞凋亡 ,是其脑保护作用的分子机制之一。
Objective To study the brain protective effect and its molecular mechanism of Danakang in focal cerebral ischemia-reperfusion injury in rats. Methods The model of middle cerebral artery (MCAO) ischemia was established by thread occlusion for 1 hour and then reperfusion for 24 hours. Eighteen male rats were randomly divided into sham operation group, saline control group and Danacan treatment group only. The degree of neurological deficit was observed by Zea Longa scoring method. The expression of P53 protein and apoptosis were observed by immunohistochemical method and TUNEL method. Results The neurological deficit score was 0 in sham operation group and no positive staining of P53 protein and apoptotic cells in high power field. The score of neurological deficit (0.48 ± 0.30) and P53 protein The number of positive staining cells (5.16 ± 1.84 / high power field) and the number of apoptotic cells (4.18 ± 1.2 1 / high power field) were significantly higher than those in saline control group (2.76 ± 0.82, 4 3 ± 1.5 6 / high power field, 8.16 ± 1.5 0 / high power field) was significantly decreased (P <0.01). Conclusion Danakang can obviously reduce the focal cerebral ischemia-reperfusion injury, which inhibits the expression of P53 protein in neurons, and then inhibits the apoptosis. It is one of the molecular mechanisms of brain protection.