NS398对Aβ肽损伤原代培养海马神经元的影响

The effect of NS398 on primary cultured hippocampal neurons injured by β-amyloid peptide

目的:探讨Cox-2抑制剂NS398对损伤神经元的保护作用。方法:将原代培养的SD大鼠海马神经元随机分为空白对照组、Aβ肽细胞模型组和NS398实验组。以10μmol/L Aβ25-35制作原代培养海马神经元损伤模型,以四氮唑溴盐(MTT)比色法检测细胞存活率,免疫细胞化学法检测Cox-2、Caspase-3的表达。结果:Aβ25-35细胞模型组神经元形态变化明显,细胞存活率明显下降,Cox-2和Caspase-3表达增强,与空白组比较有显著差异(P<0.01)。NS398使神经元细胞存活率明显提高并使Cox-2和Caspase-3表达减弱,与Aβ肽模型组比较具有显著性差异(P<0.01)。结论:Aβ25-35导致Cox-2和Caspase-3的表达增强,并使SD大鼠原代培养海马神经元变性、死亡。NS398可能通过抑制Cox-2和Caspase-3的表达保护原代培养海马神经元。

Objective： To investigate the effect of NS398, an inhibitor of Cox-2, in protecting the injured neurons. Methods： The SD rat primary cultured hippocampal neurons were randomly divided into blank control group, Aβ peptide injury model group and NS398 experimental group. 10 μmol/L Aβ25-35 was added to the primary cultured hippocampal neurons to make the injury model. MTT test was used to examine the rates of cell viability. The expression of Cox-2 and Caspase-3 was examined by immunocytochemistry. Results： In Aβ peptide injury model group, the morphology of neu- rons changed obviously, and the viability of neurons decreased dramatically, the expression of Cox-2 and Caspase-3 in- creased, it was significantly different compared with the blank control group（ P 〈 0.01 ）. Compared with the Aβ peptide injury model group, the neuronal viability increased significantly, and the expression of Cox-2 and Caspase-3 significantly decreased in NS398 group（ P 〈 0.01 ）. Conclusion： Aβ25.s5 can increase the expression of Cox-2 and Caspase-3 in prima- ry cultured hippoeampal neurons and induce the denaturation and death of these neurons. NS398 might protect the primary cultured hippocampal neurons by inhibiting the expression of Cox-2 and Caspase-3.