实验性脑出血后细胞凋亡与神经损伤的关系

The relationship between apoptosis and neurological impairment in experimental intracerebral hemorrhage in rats

目的探讨脑出血后血肿周围组织细胞凋亡、Bcl-2和Bax蛋白表达与神经功能损伤的关系。方法SD大鼠70只,随机分为实验组和对照组,每组各35只。实验组采用胶原酶诱导尾状核脑出血模型,分别于术后6 h、12 h、24 h、48 h、72 h、7 d、14 d共7个时相点(每个时相点5只)评测其神经功能缺损情况。之后处死大鼠,采用TUNEL法、免疫组化SP技术,检测血肿周围脑组织细胞凋亡及Bcl-2,Bax蛋白的表达。结果脑出血后大鼠出现不同程度的神经功能缺损,以术后48 h左右损害严重,出血后6 h血肿周围组织出现TUNEL阳性细胞,48 h达高峰。Bcl-2和Bax蛋白表达高峰期分别是脑出血术后6 h和48 h。结论脑出血后细胞凋亡与神经损伤程度一致,细胞凋亡在脑出血后神经功能损伤中起重要作用。

Objective To investigate the relationship between the apoptosis, expressions of Bcl-2 and Bax protein in perihematomal brain regions of rats and neurologic dysfunctions after intracerehral hemorrhage （ICH）. Methods Seventy Sprague-Dawley rats were divided randomly into two groups： an experimental group and a control group. A model of ICH was established by injection of 0.5 U bacterial collagenase Ⅶ into the caudate nucleus in the rats. Neurological impairment was evaluated at 6 h, 12 h, 24 h, 48 h, 72 h, 7 d and 14 d after ICH, respectively, before the rats were sacrificed. TUNEL method was used to detect apoptosis, and SP method to detect expressions of Bcl-2 and Bax protein in the perihematomal brain tissues. Results Neurological impairment occurred in all the rats after ICH, and peaked at 48 h after ICH. The apoptosis and expressions of Bcl-2 and Bax protein were peaked at 48 h, 6 h and 48 h after ICH, respectively. Conclusion The degree of the neurological impairment after ICH is parallel to that of the apoptosis. Apoptosis may play an important role in neurological impairment after ICH.