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目的探讨阿魏酸钠(sodium ferulate,SF)对一氧化氮(NO)供体硝普钠(SNP)引起的大鼠海马神经元凋亡及NF-κBP65、par-4基因表达的影响。方法采用SD大鼠海马神经元原代培养,经终浓度分别为10、20、40、80、120、160μmol/L的SF预处理后,用50μmol/L的SNP处理24h,采用MTT法检测细胞存活率,Hochest33258荧光染色检测凋亡,Westernblot及RT-PCR检测NF-κBP65、par-4基因表达。结果不同剂量SF(10～160μmol/L)预处理6h可显著提高神经元的存活率,减少SNP引起的核固缩、凝聚和碎裂现象;降低NF-κBP65、par-4mRNA及蛋白的表达。结论SF抑制NO供体SNP诱导的海马神经元凋亡,其机制可能与降低促凋亡基因NF-κBP65、par-4表达有关。
Objective To investigate the effect of sodium ferulate (SF) on apoptosis of rat hippocampal neurons and expression of NF-κB P65 and par-4 genes induced by nitric oxide (NO) donor sodium nitroprusside (SNP). Methods Sprague-Dawley rat hippocampal neurons were cultured in primary culture and pretreated with SF at final concentrations of 10, 20, 40, 80, 120, and 160 μmol/L, and treated with 50 μmol/L SNP for 24 h. Cells were detected by MTT assay. The survival rate was detected by fluorescence staining with Hochest33258, and the expression of NF-κB P65 and par-4 genes was detected by Western blot and RT-PCR. Results Different doses of SF (10-160 μmol/L) pretreatment for 6 h could significantly increase the survival rate of neurons, reduce the phenomenon of nuclear condensation, aggregation and fragmentation caused by SNPs, and decrease the expression of NF-κB P65 and par-4 mRNA and protein. Conclusion SF can inhibit the apoptosis of hippocampal neurons induced by NO donor SNP. The mechanism may be related to the decrease of pro-apoptotic genes NF-κB P65 and par-4 expression.