Effect of cyclooxygenase 2 on hippocampal neuronal damage induced by aluminum in rats

AIM:To study the relationship between cyclooxygenase 2(COX-2) and the damage of hippocampal neurons by aluminum overload in rats. METHODS:Newborn SD rats(less than 24 h) were used to establish the model of primary culture of hippocampal neurons. The neurons were treated with aluminum at concentration of 200 μmol/L. The techniques of RNA interference(RNAi) and cell transfection were used to study the role of COX-2 in hippocampal neuron. Following RNAi by cell transfection, Western blotting analysis was used to determine the protein expression of COX-2. Cell growth was assayed by the method of MTT. The pathological changes of the neurons were observed by fluorescence labeling. The activity of superoxide dismutase(SOD) and lactate dehydrogenase(LDH), and the content of malondialdehyde(MDA) were detected for evaluating cell damage. RESULTS:COX-2 RNAi by cell transfection significantly decreased the protein expression of COX-2 without changing the neuronal pathomorphology, cell viability, SOD activity and MDA content. However, it obviously improved livability and SOD activity of the hippocampal neurons, which were aluminum-overloaded. Inhibition of COX-2 expression also reduced the leakage of LDH and the content of MDA, and ameliorated the pathological changes in neurons. CONCLUSION:Moderate silence of COX-2 expression not only significantly affects the morphological changes and physiological functions of hippocampal neurons, but also prevents the neurons from aluminum-induced damages.