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目的:探讨染料木素对铅诱导的细胞毒性的影响。方法:PC12细胞分为对照组、染铅组、染料木素组以及铅加染料木素组;MTT实验检测细胞活力的改变,流式细胞仪检测细胞凋亡水平的变化,荧光探针检测线粒体形态的改变,Western blot方法检测线粒体融合分裂相关蛋白表达水平的变化。结果:铅可诱导PC12细胞活力的下降以及细胞凋亡率的显著增高,染料木素可抑制铅的这些毒性效应。与此同时,铅可诱导线粒体形态的损伤性改变,线粒体融合减少,分裂增多;而加入染料木素之后,线粒体损伤程度显著下降,线粒体分裂减少,融合增多。此外,线粒体融合相关蛋白Mfn2的水平在铅暴露后显著下降,而线粒体分裂相关蛋白Drp1的水平在铅暴露后显著升高,染料木素干预后均有所恢复。结论:染料木素可抑制铅诱导的PC12细胞毒性,其作用可能与其对线粒体融合分裂过程的干预有关。
Objective: To investigate the effect of genistein on lead-induced cytotoxicity. Methods: PC12 cells were divided into control group, lead group, genistein group and lead plus genistein group. The changes of cell viability were detected by MTT assay. The changes of cell apoptosis were detected by flow cytometry. The mitochondria Morphological changes were detected by Western blot analysis of mitochondrial fusion division-related protein expression level changes. Results Lead decreased the viability of PC12 cells and markedly increased the apoptosis rate. Genistein could inhibit these toxic effects of lead. At the same time, lead can induce the damage of mitochondrial morphology, reduce the mitochondrial fusion and increase the division. After adding genistein, the degree of mitochondrial damage decreased significantly, the mitochondrial mitosis decreased and the fusion increased. In addition, the level of mitochondrial fusion-related protein Mfn2 decreased significantly after exposure to lead, while the level of mitochondrial cleavage-associated protein Drp1 increased significantly after lead exposure, with restoration of genistein after intervention. Conclusion: Genistein can inhibit lead-induced PC12 cytotoxicity, which may be related to the mitochondrial fusion and mitotic process intervention.