CAJ | 학술논문

目的：探讨香烟烟雾暴露对小鼠长时程增强（ LTP）效应的影响；及烟草提取液（ CSE）对原代培养的小鼠海马神经轴突生长和神经元存活的影响。方法将小鼠按1d、1w、2w、4w和8w不同时间进行香烟烟雾暴露染毒，采用神经电生理技术检测小鼠海马突触传递LTP效应的变化；原代培养小鼠海马神经元，用35μg/ml、14μg/ml、4μg/ml、0. 4μg/ml和0.04μg/ml 五个终浓度的CSE对细胞进行干预，24 h后观察细胞形态变化；采用四甲基偶氮唑盐（ MTT）实验观察细胞活力，流式细胞术检测神经细胞凋亡，彗星实验检测神经细胞DNA的损伤。结果烟雾暴露1 d的小鼠群峰电位（ PS）增强幅度与对照组相比无明显改变；烟雾暴露1 w和2 w的小鼠PS增强幅度较对照组降低；随着烟雾暴露时间延长，4 w和8 w组小鼠PS增强幅度明显增高（ P ﹤0.05）。给予CSE处理的神经细胞随着CSE浓度的降低，神经细胞凋亡率呈递减趋势。CSE对神经细胞未产生DNA链断裂等作用，无DNA损伤效应。结论香烟烟雾暴露1~2 w的小鼠神经突触可塑性及神经元的兴奋性降低；烟雾暴露时间延长至4~8 w，小鼠神经突触可塑性及神经元的兴奋性随之增强。CSE对神经细胞未见明显的损伤作用。
목적：탐토향연연무폭로대소서장시정증강（ LTP）효응적영향；급연초제취액（ CSE）대원대배양적소서해마신경축돌생장화신경원존활적영향。방법장소서안1d、1w、2w、4w화8w불동시간진행향연연무폭로염독，채용신경전생리기술검측소서해마돌촉전체LTP효응적변화；원대배양소서해마신경원，용35μg/ml、14μg/ml、4μg/ml、0. 4μg/ml화0.04μg/ml 오개종농도적CSE대세포진행간예，24 h후관찰세포형태변화；채용사갑기우담서염（ MTT）실험관찰세포활력，류식세포술검측신경세포조망，혜성실험검측신경세포DNA적손상。결과연무폭로1 d적소서군봉전위（ PS）증강폭도여대조조상비무명현개변；연무폭로1 w화2 w적소서PS증강폭도교대조조강저；수착연무폭로시간연장，4 w화8 w조소서PS증강폭도명현증고（ P ﹤0.05）。급여CSE처리적신경세포수착CSE농도적강저，신경세포조망솔정체감추세。CSE대신경세포미산생DNA련단렬등작용，무DNA손상효응。결론향연연무폭로1~2 w적소서신경돌촉가소성급신경원적흥강성강저；연무폭로시간연장지4~8 w，소서신경돌촉가소성급신경원적흥강성수지증강。CSE대신경세포미견명현적손상작용。
Objective To explore the influence of passive smoking in different periods on LTP and the neural mechanism of mice,and to demonstrate the effect of cigarette smoke extractant( CSE)in different concentrations on the growth of primitive culture of hippocampal neurons of mice. Methods Models of passive smoking were established in different exposure periods(1 day,1 week,2 weeks,4 weeks and 8 weeks),and the effect of hippocampal synaptic long-term potentiation had been studied. Primitive hippocampal neurons of mice were cultured and evaluated. Morphological features,MTT assay and neuron apoptosis were tested by flow cytometry,DNA damage in neuron was tested by comet assay when neurons were exposed to CSE with different ending concentrations(35 μg/ml,14 μg/ml,4 μg/ml,0. 4 μg/ml and 0. 04 μg/ml). Results PS range of passive smoking in 1d group had no obvious change compared with control group,PS range of passive smoking in 1w and 2w groups were lower than those of control group,PS ranges of passive smoking in 4w and 8w groups were obviously higher( P ﹤0. 05). Apoptosis of neurons treated with CSE was lower than that of control group. Neurons treated with decreasing concentration of CSE,showed a trend of decline in rate of apoptosis. DNA damage had not been found in neurons. Conclusion Short-term smoking inhibited the formation of LTP in hippocampal dentate gyrus and CA1 areas,but with increasing in smoking period,suggested that long-term passive smoking can lead to increase the excitability of nerve cells and plasticity of nerve synapse. CSE had no injurious effect on neurons.