Anti-microRNA-132 causes sevoflurane‑induced neuronal apoptosis via the PI3K/AKT/FOXO3a pathway.
Anti-microRNA-132 causes sevoflurane‑induced neuronal apoptosis via the PI3K/AKT/FOXO3a pathway.
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DOI：
10.3892/ijmm.2018.3895
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发表时间：
2018-12
影响因子：
5.4
通讯作者：
Yang B
中科院分区：
文献类型：
--
作者：
Dong P;Zhang X;Zhao J;Li D;Li L;Yang B
本研究探讨了microRNA-132(miRNA-132)对七氟醚诱导的神经细胞凋亡的保护作用机制。用逆转录-定量聚合酶链式反应和基因芯片杂交分析microRNA水平的变化。用四甲基偶氮唑盐比色法、流式细胞仪和caspase-3/9活性检测试剂盒检测细胞存活率、细胞凋亡率和caspase-3/9活性。免疫荧光染色和Western印迹分析检测磷脂酰肌醇3-激酶(PI3K)和磷酸化(p-)AKT，叉头盒O3a(FOXO3a)的蛋白表达。与阴性对照组相比，七氟醚诱导的大鼠脑内miRNA-132的表达下调。在七氟醚诱导的体外模型中，miRNA-132的下调增加了神经细胞的凋亡，而miRNA-132的上调抑制了神经细胞的凋亡。在七氟醚诱导的体外模型中，miRNA-132的下调抑制了PI3K和p-AKT的蛋白表达，并抑制了FOXO3a的蛋白表达。在七氟醚诱导的体外模型中，PI3K抑制剂通过AKT/FOXO3a通路增加了抗miRNA-132对神经细胞凋亡的影响。在七氟醚诱导的体外模型中，FOXO3a的促进作用通过AKT/FOXO3a途径抑制了抗miRNA-132对神经细胞凋亡的影响。提示miRNA-132通过抑制PI3K/AKT/FOXO3a通路诱导七氟烷诱导的神经细胞凋亡。
In the present study, the mechanisms underlying the protective effects of microRNA-132 (miRNA-132) on sevoflurane-induced neuronal apoptosis were investigated. Reverse transcription-quantitative polymerase chain reaction and gene microarray hybridization were used to analyze alterations in microRNA levels. Cell viability, apoptosis and caspase-3/9 activity were measured using MTT, flow cytometry and caspase-3/9 activity kits. Immunofluorescence staining and western blot analysis were used to measure protein expression of phosphoinositide 3-kinase (PI3K) and phosphorylated (p-)AKT, forkhead box O3a (FOXO3a). In sevoflurane-induced rats, the expression of miRNA-132 was downregulated, compared with that in negative control rats. The downregulation of miRNA-132 increased neuronal apoptosis and the upregulation of miRNA-132 inhibited neuronal apoptosis in the sevoflurane-induced in vitro model. The downregulation of miRNA-132 suppressed the protein expression of PI3K and p-AKT, and suppressed the protein expression of FOXO3a in the sevoflurane-induced in vitro model. The PI3K inhibitor increased the effects of anti-miRNA-132 on neuronal apoptosis through the AKT/FOXO3a pathway in the sevoflurane-induced in vitro model. The promotion of FOXO3a inhibited the effects of anti-miRNA-132 on neuronal apoptosis through the AKT/FOXO3a pathway in the sevoflurane-induced in vitro model. These data suggested that miRNA-132 caused sevoflurane-induced neuronal apoptosis via suppression of the PI3K/AKT/FOXO3a pathway.
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影响因子：
5
作者：
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通讯作者：
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影响因子：
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作者：
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影响因子：
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