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目的:探讨药用纳米SiO2对人正常肺细胞MRC-5的生长抑制与氧化损伤作用。方法:纳米SiO2暴露于MRC-5细胞48h后,以MTT法测定其对细胞增殖的影响,HE染色观察细胞的形态学变化,并检测暴露后细胞内活性氧(ROS)和还原型谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)活性的改变,分析纳米材料对MRC-5细胞的氧化损伤作用。结果:两种尺度(粒径21.6、48.6nm)纳米SiO2暴露浓度分别达到0.4mg/mL与1.0mg/mL以上时,细胞存活率随暴露剂量的增加而降低,IC50分别为0.8mg/mL和1.9mg/mL。细胞形态皱缩,核质凝聚。细胞内活性氧明显升高(P<0.01),GSH含量和SOD活性显著降低(P<0.05),且呈现明显的剂量效应关系。结论:较高浓度纳米SiO2直接暴露可抑制人正常肺细胞MRC-5的增殖,其机理与细胞的氧化损伤有关。
Objective: To investigate the effect of medicinal nano-SiO2 on the growth inhibition and oxidative damage of human normal lung cell MRC-5. Methods: After exposure to nano-SiO2 for 48h, the cell proliferation was measured by MTT assay. The morphological changes of cells were observed by HE staining. The levels of intracellular reactive oxygen species (ROS) and reduced glutathione (GSH) content and the activity of superoxide dismutase (SOD), the effect of nanomaterials on the oxidative damage of MRC-5 cells was analyzed. Results: The cell viability decreased with the increase of exposure dose with the exposure of 0.4mg / mL and 1.0mg / mL respectively at two scales (particle size 21.6 and 48.6nm) with IC50 of 0.8mg / mL and 1.9 mg / mL. Cell morphology shrinkage, nuclear condensation. The level of reactive oxygen species (ROS) in the cells was significantly increased (P <0.01), GSH content and SOD activity were significantly decreased (P <0.05), and showed a dose-dependent effect. Conclusion: Direct exposure of higher concentration of nano-SiO2 can inhibit the proliferation of human normal lung cell MRC-5, the mechanism of which is related to the oxidative damage of cells.