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目的观察苯甲酸钠(sodium benzoate,SB)对PC12肾上腺嗜铬细胞瘤细胞增殖的抑制作用及在此条件下细胞MAPKs信号通路活化表达的特点,为进一步了解SB的神经毒性及相关的分子机制提供实验依据。方法大鼠PC12细胞在含0~50 mmol/L浓度SB的培养基中培养24 h后,噻唑蓝(MTT)比色法检测细胞活性;Western blot检测JNK和ERK磷酸化水平的改变。结果 SB可呈一定的时间和浓度依赖性抑制PC12细胞增殖,其中40 mmol/L SB作用24 h对PC12细胞的抑制率为47.81%±5.23%;Western blot结果显示,SB处理可增加JNK的磷酸化水平并降低基础的ERK磷酸化水平;预孵SP600125 30 min后再加入SB,则能短暂降低JNK的磷酸化水平。结论 SB能够明显抑制PC12细胞的增殖,JNK和ERK信号转导通路可能参与了SB对PC12细胞的毒性作用机制。
Objective To observe the inhibitory effect of sodium benzoate (SB) on the proliferation of PC12 adrenal pheochromocytoma cells and the activated expression of MAPKs signaling pathway under these conditions, and to provide experimental evidence for further understanding of the neurotoxicity of SB and related molecular mechanisms in accordance with. Methods Rat PC12 cells were cultured for 24 h in medium containing 0-50 mmol / L SB, MTT assay was used to detect the cell viability. Western blot was used to detect the phosphorylation of JNK and ERK. Results SB inhibited the proliferation of PC12 cells in a time-and concentration-dependent manner. The inhibition rate of SB with 40 mmol / L SB was 47.81% ± 5.23% at 24 h. Western blot results showed that SB inhibited the phosphorylation of JNK And reduce basal levels of ERK phosphorylation. Preincubation of SP600125 for 30 min followed by addition of SB decreased transiently phosphorylation of JNK. Conclusion SB can significantly inhibit the proliferation of PC12 cells, and JNK and ERK signal transduction pathways may be involved in the toxic mechanism of SB on PC12 cells.