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作 者:曾洋[1] 李清钊[1] 岳宗恺[2] 蒋守芳[1] 郑国颖[1] 王茜[1] 张艳淑[1]
机构地区:[1]河北联合大学公共卫生学院,河北唐山063000 [2]南开大学环境科学与工程学院
出 处:《环境与健康杂志》2014年第8期673-676,F0003,共5页Journal of Environment and Health
基 金:国家自然科学基金(81102083)
摘 要:目的探讨氟对原代培养海马神经元的细胞活性及突触素(SYN)和生长相关蛋白GAP-43表达的影响。方法将原代培养的新生SD大鼠海马神经元分别暴露于含0.0、0.1、0.2、0.4、0.8μg/ml氟化钠的培养基中培养24 h。检测海马神经元的细胞活性、细胞培养上清液中的乳酸脱氢酶(lactate dehydrtogenase,LDH)活力及海马神经元中SYN和GAP-43蛋白的表达水平。结果与对照组比较,0.4、0.8μg/ml的氟染毒组海马神经元的细胞存活率均下降(P<0.01),各染毒组细胞培养上清液中LDH的活力均升高(P<0.01);0.1μg/ml氟染毒组海马神经元中SYN蛋白的表达水平升高(P<0.01),而0.4、0.8μg/ml氟染毒组SYN蛋白的表达水平均降低(P<0.01);0.2、0.4、0.8μg/ml氟染毒组海马神经元中GAP-43蛋白的表达水平均降低,差异有统计学意义(P<0.01)。且随着Na F染毒剂量的升高,海马神经元的细胞存活率呈下降趋势,细胞培养上清液中LDH的活力呈上升趋势,海马神经元SYN蛋白的表达水平呈先上升后下降的趋势,GAP-43蛋白的表达水平呈下降趋势。结论氟染毒可降低原代培养海马神经元的生存活性并损伤原代培养海马神经元的突触可塑性。Objective To explore the effects of fluoride exposure on cell viability and expression of synaptic plasticity related protein SYN and GAP-43 in primarily cultured hippocampal neurons of rats. Methods The hippocampal neurons of newborn SD rats were cultured in vitro. The cell viability, the activity of lactate dehydrogenase(LDH) in cell culture supernatant and the protein expressions of SYN and GAP-43 were detected after the cells were incubated with sodium fluoride at the concentrations of 0.0,0.1,0.2,0.4 and 0.8 μg/ml for 24 h,respectively. Results Compared with the control group, the cell viabilities in 0.4μg/ml and 0.8 μg/ml groups decreased(P〈0.01),the activity of LDH in cell culture supernatant lactate in all fluoride-treated groups increased(P〈0.01),the SYN protein expression in 0.1 μg/ml group markedly increased(P〈0.01), decreased in 0.4 and0.8 μg/ml group(P 〈0.01),the GAP-43 protein expression obviously decreased in 0.2,0.4 and 0.8 μg/ml group(P 〈0.01).Furthermore,with the concentration of sodium fluoride exposure increased,there was an appreciable decrease in cell viability and GAP-43 protein expression,increase in the activities of LDH,GAP-43 protein expression decrease after the first rise.Conclusion Fluoride exposure can reduce the cell viability and damage the synaptic plasticity of primarily cultured hippocampal neurons.
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