环氧化酶2过表达对铝盐致大鼠海马神经元损伤的影响

Effects of COX-2 overexpression on hippocampal neuronal damage induced by aluminum in rat

目的:研究环氧化酶2(COX-2)过表达与铝盐致大鼠海马神经元损伤间的关系。方法:原代海马神经元培养7d,予以铝盐负荷(终浓度200μmol/L)建立大鼠海马神经元损伤模型,以神经元转染COX-2过表达腺病毒(MOI=100),Western Blot检测COX-2的蛋白表达水平,酶化学法检测海马神经元超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、乳酸脱氢酶(LDH)漏出率及MTT值,倒置荧光显微镜观察海马神经元病理形态变化。结果:COX-2过表达腺病毒转染的神经元COX-2蛋白表达增加(P<0.01),SOD活性、MDA含量、LDH漏出率、MTT值,以及大鼠海马神经元细胞的形态和结构未见明显异常变化。而COX-2过表达腺病毒转染在铝盐负荷基础上的海马神经元细胞MTT值和SOD活性明显下降,LDH漏出率和MDA含量明显上升(P<0.01或P<0.05),表现为严重的细胞损伤。结论:单纯的一定程度COX-2过表达不会造成神经元明显损伤,但可增加神经元对铝盐损伤的敏感性。

AIM： To study the relationship between COX-2 overexpression and hippocampal neuronal damage induced by aluminum. METH-ODS： Neonatal SD rats less than 24 h were used to establish the model of primary cultured hipp-ocampal neuron treated aluminum overload（200 μmol/L）. The primary cultured hippocampal neurons were transfected by adenovirus over ex- pressing COX-2. The expression of COX-2 pro-tein in hippocampal neurons was measured by Western Blot. The SOD and LDH activities and MDA contents were detected respectively. The cell viability was measured by MTT. The fluo-rescence detection was used to observe the change of neuronal pathomorphology. RE-SULTS： The transfection of adenovirus overex- pressing COX-2 significantly increased the ex- pression of COX-2 protein （P〈 0.01 ）, without effects on neuronal pathomorphology, cell via- bility, the SOD activity and MDA content. However, it remarkably increased damage to neurons induced by aluminum overload. CON-CLUSION： Acertain degree of COX-2 overex- pression may not cause serious injury of neu- rons, but can increase the damage susceptibility of neurons undergoing aluminum overload.