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目的研究硫辛酸对氧化应激的PC12细胞NF-κB-iNOS-NO信号通路的影响。方法用终浓度为0.4mmol·L-1的H2O2损伤PC12细胞,用MTT法测定细胞存活率;用激光共聚焦法(LSCM)检测细胞内一氧化氮的动态变化;用RT-PCR法检测iNOS mRNA和NF-κBp65 mRNA表达量的变化。结果0.4mmol·L-1的H2O2处理PC12细胞4h,细胞存活率为27.9%(P<0.01),硫辛酸10mg·L-1可以提高H2O2损伤的PC12细胞存活率(65.4%,P<0.01);LSCM检测显示,DAF-2荧光强度的比值(Ft/F0)的最大值由损伤模型组的5.34下降到1.80;和模型组比较,iNOS mRNA和NF-κB p65 mRNA的表达明显下调(P<0.05或P<0.01)。结论硫辛酸可能通过抑制NF-κB-iNOS-NO信号减轻氧化应激诱导的PC12细胞损伤。
Objective To investigate the effect of lipoic acid on oxidative stress-induced NF-κB-iNOS-NO signaling in PC12 cells. Methods PC12 cells were injured by H2O2 at a final concentration of 0.4mmol·L-1, and the cell viability was measured by MTT assay. The changes of intracellular nitric oxide were detected by laser scanning confocal microscopy (LSCM). The expression of iNOS Changes of mRNA and NF-κBp65 mRNA expression. Results PC12 cells were treated with 0.4mmol·L -1 H2O2 for 4h, the cell survival rate was 27.9% (P <0.01). Lipoic acid 10 mg · L-1 could increase the survival rate of PC12 cells (65.4%, P <0.01) ; LSCM showed that the maximum value of Ft / F0 ratio of DAF-2 decreased from 5.34 to 1.80 in model group, and the expression of iNOS mRNA and NF-κB p65 mRNA was significantly decreased in model group (P < 0.05 or P <0.01). Conclusion Lipoic acid may reduce oxidative stress-induced PC12 cell injury by inhibiting NF-κB-iNOS-NO signaling.