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本文以PC12细胞为神经细胞模型,研究了西维因对神经细胞的损伤作用机理。当PC12细胞暴露于0.00μg/m L~200.00μg/m L不同浓度的西维因溶液时,表现出了一系列显著变化。随着西维因溶液浓度的增大,细胞的存活率从(100.00±0.46)%下降到了(27.86±1.69)%;细胞内乳酸脱氢酶(LDH)漏出率增多;丙二醛(MDA)含量从19.27±0.96 nmol/mg prot逐渐增加到112.39±1.59nmol/mg prot;超氧化物歧化酶(SOD)活力从4.08±0.87 U/mg prot增强到17.77±0.43 U/mg prot,同时其抑制率也从(19.00±1.66)%增加到了(73.00±1.71)%;同时谷胱甘肽(GSH)含量从96.15±6.10μmol/g prot逐渐减少到22.91±3.98μmol/g prot;细胞相对荧光强度(RFI)从37.38±11.48先增强到45.56±11.96,后因细胞严重损伤又减弱到17.11±1.50。细胞液内乙酰胆碱(ACh)含量也逐渐增加。同时,利用激光共聚焦扫描显微镜观察到了线粒体膜电位的显著下降。西维因对PC12细胞表现出很强的神经毒性。
In this paper, PC12 cells as a model of neural cells to study the mechanism of the injury of neurons caused by Cimetidine. PC12 cells showed a series of significant changes when exposed to different concentrations of the Cimetidine solution ranging from 0.00 μg / mL to 200.00 μg / mL. The cell viability decreased from (100.00 ± 0.46)% to (27.86 ± 1.69)% with the increase of the solution concentration of cisplatin, and the leakage rate of intracellular lactate dehydrogenase (LDH) increased. The malondialdehyde (MDA) The content of SOD increased from 19.27 ± 0.96 nmol / mg prot to 112.39 ± 1.59 nmol / mg prot. The activity of superoxide dismutase increased from 4.08 ± 0.87 U / mg prot to 17.77 ± 0.43 U / mg prot, (19.00 ± 1.66)% to (73.00 ± 1.71)%, while the content of glutathione (GSH) decreased from 96.15 ± 6.10μmol / g prot to 22.91 ± 3.98μmol / g prot. The relative fluorescence intensity (RFI) increased from 37.38 ± 11.48 to 45.56 ± 11.96, and then weakened to 17.11 ± 1.50 due to severe cell injury. The amount of acetylcholine (ACh) in the cytosol also gradually increased. At the same time, a significant decrease in mitochondrial membrane potential was observed using a confocal laser scanning microscope. Cvvine shows strong neurotoxicity on PC12 cells.