摘要
目的应用原代培养胎鼠海马神经元,观察双苯氟嗪对β-淀粉样肽25～35(Aβ25～35)诱导神经元损伤的保护作用。方法原代培养的海马神经元分别与1.0μmol/Lβ25～35、双苯氟嗪(0.1、1、10μmol/L)孵育24h后,检测细胞内漏出液的谷胱甘肽过氧化酶(GSH-Px)活性、丙二醛(MDA)含量、超氧化酶歧化酶(SOD)活性及细胞存活率的变化。结果海马神经元与β25～35共同孵育24h后,细胞存活率显著下降、GSH-Px及SOD活性降低、MDA含量升高;海马神经元与不同浓度双苯氟嗪共同孵育24h后,细胞存活率显著升高、GSH-Px及SOD活性升高、MDA含量降低。结论双苯氟嗪可对抗β25～35所造成的神经元损伤,该作用可能与通过清除氧自由基、提高神经元的抗氧化能力有关。
Objective To study the protective effect of dipfluzine on cultured hippocampal neurons injury induced by β-amyloid peptide 25 - 35 （ Aβ -35 ）- Methods After hippocampal neurons were incubated with Aβ25 -35 （ 1.0 umol/L）, dipfluzine for 24 h, respectively, the neurons surviving rate, the activities of glutathione peroxidase （GSH-Px） and superoxide dismutase （ SOD）, content of maleic dialdehyde （MDA） were measured. Results When hippocampal neurons were incubated with Aβ25 - 35 for 24 h, the neurons surviving rate was decreased remarkably, activities of GSH-Px and SOD were suppressed, and the content of MDA was increased. After dipfluzine was used to incubate for 24 h, the surviving rate of hippocampal neurons was increased, the activities of GSH-Px and SOD were increased and the content of MDA was decreased compared with Aβ25 -35 treating group. Conclusions Dipfluzine possesses protective effects against injury of hippocampal neurons induced by Aβ25 - 35, which is related to anti-liped peroxidation via free-radical scavenging activity.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2010年第13期1826-1828,共3页
Chinese Journal of Gerontology
基金
国家863高新技术研究发展计划资助项目(2002AA2z3132)
河北医科大学科研骨干人才培育计划(2007003)
