摘要
目的观察刺五加(AS)对脑出血(ICH)大鼠脑细胞凋亡及其对凋亡调控蛋白Bcl-2、Bax的影响及对ICH脑组织的保护作用。方法雄性Wistar大鼠随机分为正常组、假手术组、模型组与治疗组。治疗组又分为AS大剂量组和小剂量组。用胶原酶注入大鼠尾状核建立ICH模型。治疗组给予AS干预,在不同时间点处死大鼠,测定血肿周围组织细胞凋亡、Bcl-2和Bax水平。结果 AS治疗组分别于12h、1、3、7d凋亡细胞低于模型组(P<0.01,P<0.05)。AS治疗组Bcl-2水平分别于12h、1、3、7d表达高于模型组(P<0.01,P<0.05)。Bax于12h、1、3、7d时AS治疗组表达低于模型组(P<0.01,P<0.05)。结论 AS能明显减少ICH后神经细胞凋亡,升高Bcl-2表达水平,降低Bax表达,保护ICH后神经细胞。
Objective To observe the effects of Acanthopanax senticosus （AS） on brain apoptosis and expression of Bcl-2,Bax protein in rats after intracerebral hemorrhage （ICH） and explore the protective mechanism of AS on neural cell. Methods Male Wistar rats were divided randomly into normal,model,sham operated and therapy groups. The therapy group included high-and low-dose AS therapy groups. Models of ICH were established on local injection of collagenase into caudate nucleus. The therapy group rats were treated with AS. Rats of all groups were killed at specific times and apoptosis level and the change of Bcl-2,Bax were detected. Results Apoptosis cells in therapy group were significantly decreased compared with that of model group at 12 h,1,3 and 7 d （P0.01,P0.05）. The expression of Bcl-2 protein in therapy group were significantly increased compared with that of model group at 12 h,1,3 and 7 d （P0.01,P0.05）. The expression of Bax protein in therapy group were significantly increased compared with that of model group at 12 h,1,3 and 7 d （P0.01,P0.05）. Conclusions AS could greatly reduce the amount of apoptosis cells after ICH,which probably relates to high expression of Bcl-2 protein and lower expression of Bax protein.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2010年第19期2788-2791,共4页
Chinese Journal of Gerontology
基金
贵州省卫生厅资助项目(No.D-288)
关键词
脑出血
刺五加
细胞凋亡
BCL-2
BAX
Intracerebral hemorrhage
Acanthopanax senticosus
Apoptosis
TUNEL
Bcl-2
Bax
