[关键词]
[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。
[Key word]
[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.
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[基金项目]
国家科技支撑计划项目(2012BAD33B03);吉林省世行贷款农产品质量安全项目(2011-Z67);吉林大学研究生创新基金资助项目(2015052);吉林农业大学科研启动基金资助项目(2015010);国家级大学生创新创业训练计划项目(201510193002)