摘要
目的:探讨β-淀粉样蛋白(amyloid-beta protein,Aβ)对原代培养海马神经元丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力及乳酸脱氢酶(LDH)漏出量的影响及葛根素与川芎嗪合用对Aβ25-35诱导神经元损伤的保护作用。方法:通过Aβ25-35诱导体外培养的海马神经元,建立阿尔茨海默(AD)细胞模型,检测空白组(正常海马神经元)、模型组、脑复康组(终浓度为50μmol·L^-1)、川芎嗪组(终浓度为50μmol·L^-1)、葛根素组(终浓度为60μmol·L^-1),川芎嗪加葛根素组(葛根素注射液终浓度为30μmol·L^-1,川芎嗪注射液终浓度为25μmol·L^-1)对海马神经元SOD活性、MDA含量及LDH漏出量的影响。结果:成功建立海马神经元AD细胞模型,经检测模型组MDA含量及LDH漏出量显著高于空白对照组且SOD活力明显低于空白对照组,差异具有显著意义(P〈0.01);脑复康组、川芎嗪加葛根素组MDA含量及LDH漏出量均低于模型组,且SOD活力明显高于模型组,差异均具有显著意义(P〈0.01);川芎嗪与葛根素合用组在降低MDA含量及LDH漏出量及提高SOD活性方面的效果显著强于川芎嗪与葛根素单用,差异具有显著意义(P〈0.01)。结论:Aβ25-35诱导海马神经元存在自由基损伤,葛根素、川芎嗪能抗自由基损伤,对神经元具有保护作用,且二者合用在抗自由基损伤上具有协同作用。
Objective: To investigate the changes of MDA, SOD, LDH of cultured hippocampal neurons injury induced by amyloid-beta protein ( Aβ25-35) and the protective effect of puerarin and ligustrazine. Method: Primary hippocampal neurons were cultured and induced by Aβ 25-35. The concentrations of MDA, SOD and LDH in cultured hippocampal neurons were measured after ex- posed to Aβ25-35, puerarin and ligustrazine. Result: The Alzheimer disease(AD) model was successfully established in cultured hippocampal neurons. AD group has remarkably increased MDA and LDH level, and decreased SOD level, Piracetan group and combined application group of have remarkably decreased MDA and LDH level and increased SOD level, compared with AD group (P 〈 0. 01 ). Ligustrazine together with puerarin group has remarkably decreased MDA and LDH level and increased SOD level, compared with ligus-trazine group and puerarin group ( P 〈 0. 05 ). Conclusion : Aβ25-35 can induce cultured hippocampal neurons injury, combined ap- plication of ligustrazine, and puerarin can alleviate the injury.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2008年第4期424-427,共4页
China Journal of Chinese Materia Medica
基金
国家自然科学基金项目(30672652,30371789)
浙江省自然科学基金项目(Z204424,Y405171)