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目的:研究木通皂苷D对Aβ诱导损伤的PC12细胞修复作用及相关基因表达水平的影响。方法:采用MTT法测定木通皂苷D对Aβ诱导损伤的PC12细胞修复作用,采用实时荧光定量PCR仪测定木通皂苷D对A2M、ECE2基因表达的影响。结果:在15μmol.L-1的浓度下,在6,12,24,48 h时间点,Aβ25-35诱导的PC12细胞损伤的抑制率与空白组相比,差异均有极显著性(P<0.01),且24 h时抑制率最高。木通皂苷D在不同给药时间逐渐表现出细胞增殖作用,且在作用16 h后产生明显的增殖效应,差异有极显著性(P<0.01);其中木通皂苷D处理24 h的细胞增殖作用最强,差异有极显著性(P<0.01)。与空白组比较,模型组中ECE2基因和A2M基因的相对表达量明显上调;木通皂苷D不同给药时间组PC12细胞中的ECE2基因和A2M基因的相对表达量与模型组相比明显下调。结论:木通皂苷D对Aβ诱导损伤的PC12细胞具有修复作用,其机制是通过下调ECE2基因和A2M基因的相对表达量修复Aβ25-35诱导的PC12细胞损伤。
Objective: To investigate the effect of sarassoside D on Aβ-induced injury of PC12 cells and the expression of related genes. Methods: MTT method was used to determine the effect of saponin D on Aβ-induced injury of PC12 cells. Real-time fluorescence quantitative PCR was used to determine the effect of saponin D on A2M and ECE2 gene expression. Results: The inhibitory rate of Aβ25-35-induced PC12 cell injury in the concentration of 15μmol.L-1 at 6, 12, 24 and 48 h was significantly higher than that of the blank group (P < 0.01), and the highest inhibition rate at 24 h. The results showed that the effect of Atractylodis saponin D on the cell proliferation was obvious at different time points, and the proliferation was obvious after 16 h of treatment (P <0.01) The strongest effect, the difference was significant (P <0.01). Compared with the blank group, the relative expression of ECE2 gene and A2M gene in the model group was significantly increased; the relative expression of ECE2 gene and A2M gene in PC12 cells was significantly decreased compared with model group. CONCLUSION: Allicin can repair PC12 cells damaged by Aβ, and its mechanism is to repair Aβ25-35-induced PC12 cell injury by down-regulating the relative expression of ECE2 and A2M genes.