摘要
[目的]探讨铝对原代培养神经细胞的毒性作用及对代谢型谷氨酸受体3(metabotropic glutamate receptors,mGluR3)基因表达的影响。[方法]采用结晶氯化铝(AlCl3·6H2O)分别对原代培养昆明小鼠的神经细胞染毒,使其终浓度分别为0mmol/L(对照组)、0.5mmol/L(低剂量组)、1.0mmol/L(中剂量组)和2.0mmol/L(高剂量组),染毒48h后,采用CCK-8试剂盒,使用酶联免疫仪检测细胞活力,采用逆转录-聚合酶链反应(RT-PCR)法测定mGluR3基因的表达。[结果]与对照组比较,高剂量组细胞活力明显下降(P<0.05);RT-PCR测定结果显示高剂量组相对于对照组mGluR3表达量明显降低(P<0.05)。[结论]铝对原代培养的神经细胞产生细胞毒性可能与mGluR3基因表达降低有关。
[ Objective ] To investigate the toxic effects of aluminum on primary cultured neurocytes in mice and the metabotropic glutamate receptor 3 ( mGluR3 ) expression. [ Methods ] The neurocytes were treated with aluminum chloride ( AlCl3 · 6H2O )at final concentrations of 0 mmol/L( control ), 0.5 mmol/L( low-dose ), 1.0 mmol/L( medium-dose ), and 2.0 mmol/L ( high-dose ) separately; then incubated for 48 hour. The CCK-8 enzyme-linked immunosorbent assay kit was used to detect celt viability, and the expression ofmGluR3 were detected by RT-PCR. [ Results ] Compared with control group, AlCl3 decreased the viability of cultured neurocytes in high dose group significantly( P 〈 0.05 ). The RT-PCR demonstrated that mGluR3 gene expression in high dose group decreased significantly compared with control group after aluminum exposure( P 〈 0.05 ). [ Conclusion ] The cytotoxic effect of aluminum on primary cultured neurocytes in mice may be associated with the decrease of mGluR3 gene expression.
出处
《环境与职业医学》
CAS
北大核心
2010年第1期14-16,共3页
Journal of Environmental and Occupational Medicine
基金
国家自然科学基金资助项目(编号:30671777)