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作 者:郑俩燕[1] 许荣华[2] 姚茂忠[3] 蔡美华[1] 陈志斌[1]
机构地区:[1]海南医学院附属医院神经内科,海口571101 [2]海南医学院附属医院肿瘤外科,海口570102 [3]海南医学院附属医院海南省药物安全性评价研究中心,海口571101
出 处:《神经解剖学杂志》2013年第4期464-468,共5页Chinese Journal of Neuroanatomy
基 金:海南省教育厅高等学校科学研究资助项目(Hjkj2008-44)
摘 要: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.
关 键 词:细胞培养 海马神经元 Β淀粉样蛋白 半胱氨酸蛋白酶-3 环氧合酶-2
分 类 号:R338[医药卫生—人体生理学]
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