氯化铝致原代培养小鼠神经细胞毒性作用及对mGluR3表达的影响

The Toxic Effect of Aluminum Chloride on Primarily Cultured Mice Neurocytes and Gene Expression of mGluR3

  • 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& #183;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培试剂盒,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。

     

    Abstract:
    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& #183;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.

     

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