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作 者:江湧[1] 何玉萍[1] 邹衍衍[1] 方永奇[1]
机构地区:[1]广州中医药大学第一附属医院实验中心,广州市机场路16号510405
出 处:《中国康复医学杂志》2007年第6期490-491,共2页Chinese Journal of Rehabilitation Medicine
基 金:广东省自然科学基金(编号04300378);广东省中医药管理局基金(编号2040007)
摘 要:目的:探讨β-细辛醚对三氯化铝引起的痴呆小鼠脑皮质神经元凋亡的保护机制。方法:选用NIH小鼠,正常培养3个月,随机分为正常对照组,模型对照组,β-细辛醚1.06mg/100g/d组。除正常对照组给予生理盐水外,其他各组均灌胃三氯化铝,并分别给予生理盐水或β-细辛醚,计6个月。用流式细胞术测量脑皮质神经元内钙离子浓度及DNA周期分析,观察细胞的凋亡率。结果:1.06mg/100g/dβ-细辛醚组神经功能缺损较非治疗组明显减轻,相应的β-细辛醚治疗组细胞内钙离子浓度增高受抑、细胞凋亡减少。结论:1.06mg/100g/dβ-细辛醚可以减轻脑组织神经元痴呆损伤和抑制神经元凋亡;抑制受损神经元细胞内钙离子浓度增高可能是其保护作用的机制之一。Objective: To investigate the protective effect of β-asarone on calcium level and DNA content of cerebral cortex cell apoptosis induced by AlCl3 in mice. Method:Thirty NIH mice were randomized into normal group, model group, β-asarone treatment group(1.06mg/100g/d).AlCl3 injured mice was used as model of Alzheimer's disease. After three months the concentration of intracellular Ca^2+ and DNA cycle analysis were detected. Result: The concentration of intracellular Ca^2+ in model group was increased significantly compared with normal group, while decreased remarkably between β-asarone treatment group and model group. Conclusion: β-asarone has a significant relieving effect on the lesion of learning and memory in AD model mice by decease the intracellular Ca^2+ concentration and DNA apoptosis rate.
分 类 号:R749.1[医药卫生—神经病学与精神病学] R49[医药卫生—临床医学]
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