摘要
目的:观察脑心通胶囊对血管性痴呆模型大鼠海马神经细胞静息态游离Ca2+浓度([Ca2+]i)的影响,初步探讨脑心通胶囊治疗血管性痴呆的机制。方法:采用大脑中动脉闭塞法(MCAO)制作血管性痴呆动物模型;使用胰蛋白酶消化法制备海马组织单细胞悬液,Fura-2/AM负载分离的神经细胞,双波长荧光法测定海马神经细胞内静息态[Ca2+]i。结果:模型组大鼠海马神经细胞静息态[Ca2+]i为437.42±32.14nmol/L,显著高于假手术组189.83±18.57 nmol/L(P<0.05);脑心通组和喜德镇组大鼠海马神经细胞静息态[Ca2+]i为252.61±20.15 nmol/L、237.34±19.83 nmol/L,较模型组显著降低(P<0.05)。结论:脑心通胶囊可降低血管性痴呆模型大鼠海马神经细胞静息态[Ca2+]i,这可能是脑心通胶囊治疗血管性痴呆的作用机制之一。
Objective： To investigate the influence of Naoxintong Capsule on the resting [Ca^2＋]i level in hippocampal neurons of the rat modals with vascular dementia and furthemoe, to explore its therapeutic mechanism on vascular dementia. Methods： The vascular dementia model was established by occlusion of the middle cerebral artery in rats. The isolated neuron suspension was obtained by using parenzyme to digest hippocamal tissue and loaded with Fura-2/AM as fluorescence indicator, and then the resting [Ca^2＋]i was measured with double-wavelength fluoremetry. Result： The resting [Ca^2＋]i level in model group was 437.42±32.14nmol/L and significantly higher than that in the shamedoperated group（P 〈 0.05）. The resting [Ca^2＋]i levels in Naoxintong capsule group and hydergine group were separately 252.61±20.15 nmol/L, 237.34±19.83 nmol/L and there were no significant difference between these two therapy groups（P 〉 0.05）. Conclusion： Naoxintong capsule can decrease the resting [Ca^2＋]i level in hippocamal neurons in the rat models with vascular dementia and it may be one of its therapeutic mechanism on vascular dementia.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2006年第3期133-135,共3页
Pharmacology and Clinics of Chinese Materia Medica
