基于PC12细胞的西维因神经损伤作用机理研究

Mechanism of Neurotoxicity Injuries Induced by Carbaryl in PC12 Cells

摘要:

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0.00 μg/mL~200.00 μg/mL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±1.59 nmol/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±6.10 μmol/g prot逐渐减少到22.91±3.98 μmol/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。

Abstract:

The present study was planned to evaluate neurotoxicity injuries induced by carbaryl in PC12 cells, which were used as a model for nervous cell system. In this study, PC12 cells were exposed to carbaryl in different concentrations from 0.00 μg/mL to 200.00 μg/mL, and showed significant changes. Cells viability rates decreased from (100.00±0.46)% to (27.86±1.69)% with a increase of carbaryl concentration. Carbaryl treatment resulted in a significant increase in the levels of LDH leakage rate. MDA content also increased from 19.27±0.96 nmol/mg?prot to 112.39±1.59 nmol/mg prot. SOD activity increased from 4.08±0.87 U/mg prot to 17.77±0.43 U/mg prot, and SOD inhibition rate increased from (19.00±1.66)% to (73.00±1.71)%, however, GSH content decreased from 96.15±6.10 μmol/g prot to 22.91±3.98 μmol/g prot. RFI increased from 37.38±11.48 to 45.56±11.96 firstly, then decreased to 17.11±1.50 with the damage of cells. Ach in medium increased by carbaryl treatment. A significantly decrease in integrity of mitochondrial membrane potential was observed by laser scanning confocal microscope. Carbaryl can induce neurotoxicity in PC12 cells.