缺氧海马神经元中K_(ATP)对基因Bax表达的影响

Effect of K_(ATP) on gene Bax in hippocampal neurons under hypoxia treatment

目的研究缺氧海马神经元中KATP对基因Bax表达的影响。方法对原代海马神经元进行缺氧和药物处理,倒置显微镜和NF免疫组织化学法观察细胞生长和形态,MTT法检测细胞凋亡率,RT-PCR检测Bax基因mRNA表达水平。结果与单纯缺氧组比较,缺氧+二氮嗪组和缺氧+甲苯磺丁脲组的多级神经元百分率和细胞存活率差异有显著性(P<0.01)。缺氧+二氮嗪组中基因Bax的mRNA表达水平与单纯缺氧组相比下降(P<0.01),缺氧+甲苯磺丁脲组中基因Bax的mRNA表达水平相对于单纯缺氧组也有提高(P<0.05)。结论缺氧时KATP的开放对细胞具有保护作用,它通过降低Bax的表达抑制缺氧海马神经元的凋亡。

Objective To study the effect of KATP on gene Bax in hippocampal neurons under hypoxia condition. Method The neurons were exposed to hypoxia condition or treated with medicine. Inverted microscope and immunohistochemistry of NF were performed to assess the growth and morphology of the cells. Cell viability was measured with MTT cell assay. RT-PCR was used to detect expression of Bax mRNA levels. Results Compared with hypoxia groups, the percentage of multipolar neuron and survival rate of primary cultured hippocampal neurons in diazoxide and tolbutamide with bypoxia groups showed statistical difference （ P 〈 0.01 ）. The experiments showed a significant increase in Bax mRNA levels （P 〈0.01 ） in neurons cultured at severe hypoxia condition compared with those cultured at normoxia. In laypoxia groups, tolbutamide increased Bax mRNA expression （ P 〈 0.05 ） , while diazoxide reduced it （ n = 5 for each）. Conclusion The activation of KATP channels could partially reduce cell death during hypoxia. And it also indicated that KArP protects hippocampal neurons from hypoxia by suppressing Bax expression.