【摘要】 目的研究左旋丁基苯酞对β-淀粉样蛋白(Aβ)诱导的原代培养海马及基底前脑神经元损伤的保护作用。方法运用细胞原代培养的方法培养大鼠基底前脑及海马胆碱能神经元并进行鉴定,用2μmol/L的Aβ1-42建立神经细胞损伤模型,将细胞分为对照组、Aβ1-42模型组和Aβ1-42+左旋丁基苯酞(0.1、1、10μmmol/L)处理的低、中、高剂量组。倒置显微镜下观察给药前后细胞形态变化,Western Blot检测NF-κB及nNOS的含量。结果与对照组比较,Aβ1-42作用于原代神经元48 h后,神经细胞形态发生显著改变,NF-κB表达增高,nNOS表达降低(P均<0.05),低、中、高剂量的左旋丁基苯酞能够显著改善细胞形态,抑制NF-κB活化,提高nNOS的表达(P均<0.05)。结论左旋丁基苯酞对Aβ1-42诱导的原代神经元保护作用可能与其抑制NF-κB活化,上调nNOS的表达有关。更多还原

【Abstract】 Objective To investigate the neuroprotective effects of L-3-N-butylphthalide(L-NBP) on the damage of cultured primitive rat basal forebrain and hippocampus cholinergic neurons induced by beta-amyloid peptides(Aβ1-42).Methods Primitive rat basal forebrain and hippocampus neurons were cultured and evaluated.Neurocyte trauma model was established by Aβ1-42(2 μmmol/L).Neurocytes were divided into control group,Aβ1-42 model group,Aβ1-42+ l-NBP lower,middle,higher group(0.1、1、10 μmmol/L).Observing cells morphologic change in inverted microscope,and NF-κB,nNOS levels were detected by ELISA.Results Being exposed to Aβ1-42 with 48 h,neurons morphologic had significantly changed,the expression of NF-κB in the cultured neurons was increased significantly and the expression of nNOS was decreased significantly compared with the controls(P<0.05).Neurons morphologic had significantly changed with different doses of l-NBP,and l-NBP could inhibit NF-κB activation,increase the expressions of nNOS(P<0.05).Conclusion The neuroprotective effects of l-NBP on cultured neurons induced by Aβ1-42 result from adjusting the expressions of NF-κB and nNOS.更多还原