丁基苯酞对血管性痴呆大鼠记忆及海马Bcl-2、Bax的影响  被引量:6

Effects of butylphthalide on memory and the apoptosis-related protein in hippocampus of vascular dementia rats

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作  者:徐书雯[1] 刘本胜[2] 高广生[3] 张霞辉[2] 王宝萍[2] 向绍通[1] 胡方方[1] 

机构地区:[1]广东省人民医院东病区神经科广东省医学科学院广东省老年医学研究所广东省神经科学研究所,广州510080 [2]南方医科大学 [3]山东省泰安市中心医院高压氧病房

出  处:《中华老年医学杂志》2011年第6期512-515,共4页Chinese Journal of Geriatrics

摘  要:目的研究丁基苯酞(NBP)对血管性痴呆(VD)大鼠记忆、海马病理变化及抗凋亡蛋白(Bcl2)和促凋亡蚩白(Bax)蛋白表达的影响。方法采用永久性结扎双侧颈总动脉方法制备VD人鼠模型。D大鼠被随机分成假手术组、VD模型组、NBP治疗组、尼莫地平治疗组。应用Morris水迷宫检测大鼠记忆能力,苏术精-伊红(HE)染色观察海乌神经元形态,免疫组化检测海马Bcl-2和Bax的表达。结果VI)模型组与假手术组大鼠比较记忆能力显著下降,逃避潜伏期分别为(78.79121.93)s与(16.96±7.41)S(P〈0.05),海马神经元病理改变严重,免疫阳性细胞数量显著增加,其中Bax变化更为最菩(13.00±6.72与6.00±1.29,P〈0.05),Bcl2与Bax的比值较对照组明显降低;NBP治疗组与模型绀比较记忆能力显著改善,逃避潜伏期分别为(47.13±21.75)s与(78.79±21.93)s(P〈20.05),海马神经元病理形态明显改善,Bcl-2免疫阳性细胞数显著增多(33.14±8.05021.81±1.97,P〈0.05),Bax免疫阳性细胞数显著减少(32.93±4.99与43.00±6.72,P〈0.05)。NBP治疗组与尼莫地平治疗组之间比较,各项指标均无显著差异(P〉0.05)。结论NBP能改善VD大鼠记忆能力,抑制海马细胞凋亡,对VD大鼠有一定的治疗作用。Objective To study the effects of hutylphthalide (NBP) on memory and apoptosis related protein as well as neuronal pathology in hippocampus of vascular dementia (VI)) rats. Methods VD model was generated by the permanent occlusion of bilateral common carotid arteries in SI~) rats to produce the forebran ischemia. Male SD rats were randomly allocated into sham-operation group, VI) model group, NBP treatment group and nimodipine treatment group. The function of memory was lested by the Morris water maze. The neuronal pathological changes and the expression of Bel-2 and Bax proteins in the hippoeampus were observed with hematoxylin-eosin (HE) staining and Results The impaired memory of VD rats was proved 79±21.93)vs. (16.96±7.44) ,P〈0. 051 and the neuron in hippocampus was severely damaged. The decveased ratio of Bcl-2/Bax resulted from the overexprcssion of Bax proteins in V1) model group versus the sham operation group [((43.00±6.72) vs. (6.00±1.29),P〈0.05]. The treatment of NBP notably improved the memory function of VD rats and reduced the hippoeampus pathological iniury (P〈0.05). The expression of Bcl 2 protein raised [(33.14±8.05)vs. (21.81±4.97),P〈0.05] along with reduced expression of Bax protein [(32.93±4.99)vs. (43.00±6.72),P〈0.05] after NBP treatment. However, there was no significant difference in the treatment effects between nimodipine and NBP group (P〉 0.05).Conclusions NBP treatment could improve memory of VD rats and reduce the hippocampus pathological lesion by inhibiting the apoptosis related protein.

关 键 词:痴呆 血管性 海马 BCL-2相关X蛋白质 

分 类 号:R285.5[医药卫生—中药学]

 

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