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目的:研究紫外对NIH3T3细胞的影响,并探讨槲皮素对NIH3T3细胞的紫外损伤保护作用。方法:建立紫外对NIH3T3细胞的损伤模型。通过不同浓度的槲皮素(1μmol/L、10μmol/L、20μmol/L)的预处理,用MTT方法检测细胞的存活率以及激光共聚焦显微镜检测细胞内活性氧含量和线粒体膜电位变化。结果:紫外损伤后的细胞内活性氧自由基含量明显增加(p<0.05),细胞膜电位下降(p<0.05),细胞凋亡后细胞存活率下降(p<0.05);槲皮素预处理组的细胞内活性氧自由基含量、线粒体膜电位、细胞存活率都呈现出较强的剂量依赖性。结论:紫外损伤可诱导细胞内产生大量的活性氧自由基,使细胞线粒体膜电位下降,降低细胞的存活率;槲皮素预处理后,通过清除细胞内的活性氧自由基,维持细胞的线粒体膜电位,抑制细胞凋亡。
Objective: To study the effect of UV on NIH3T3 cells and to investigate the protective effect of quercetin on UV injury of NIH3T3 cells. METHODS: A model of UV damage to NIH3T3 cells was established. The pretreatment with different concentrations of quercetin (1μmol/L, 10μmol/L, 20μmol/L) was used to detect the cell survival rate by MTT assay and the changes of intracellular reactive oxygen species and mitochondrial membrane potential were detected by laser confocal microscopy. RESULTS: After UV injury, the content of reactive oxygen species in cells was significantly increased (p<0.05), the membrane potential was decreased (p<0.05), and the cell survival rate after apoptosis was decreased (p<0.05); quercetin pretreatment group The intracellular reactive oxygen species content, mitochondrial membrane potential, and cell survival rate all showed a strong dose-dependent manner. Conclusion: UV damage can induce a large number of reactive oxygen species in the cells, which can decrease the mitochondrial membrane potential and decrease the survival rate of cells. After quercetin pretreatment, the mitochondria of the cells are maintained by removing the active oxygen free radicals in the cells. Membrane potential, inhibition of apoptosis.