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探讨苯乙酸 (phenylacetic acid,PAA)对大鼠原代培养的皮质神经元的毒性作用及其作用机制。实验结果显示 ,PAA加入无血清 Neurobasal培养基可剂量依赖地损伤原代培养的皮质神经元 ,且干预培养的时间越长 ,神经元存活率越低。而同浓度 (1 .1× 1 0 -3mol/L)的 PAA对皮质神经元的损伤明显高于海马。原代培养的皮质神经元补充一氧化氮合成酶抑制剂 L- NAME、NMDA受体拮抗剂 MR- 80 1及 L型钙通道阻滞剂尼莫地平可显著地抵抗 PAA的毒性作用。以上实验结果提示 ,PAA可选择性地损伤皮质神经元 ,其毒性作用可能与 NO过量产生、兴奋性氨基酸的堆积及钙超载有关
To investigate the toxic effect and mechanism of phenylacetic acid (PAA) on primary cortical neurons in rats. The results showed that adding PAA to serum-free Neurobasal medium could damage the primary cultured cortical neurons dose-dependently, and the longer the intervention culture time, the lower the survival rate of neurons. PAA at the same concentration (1.1 × 10 -3 mol / L) significantly damaged cortical neurons compared with hippocampus. Primary cultures of cortical neurons supplemented with L-NAME, NMDA receptor antagonist MR-80 1, and L-type calcium channel blocker nimodipine significantly counteract the toxic effects of PAA. The above experimental results suggest that PAA can selectively damage the cortical neurons, and its toxicity may be related to the excessive production of NO, accumulation of excitatory amino acids and calcium overload