基于PI3K/Akt通路沉默miR-26b对妊娠期高血压胎盘滋养细胞增殖、凋亡的影响

目的 分析沉默微小RNA-26b（Micro RNA-26b，miR-26b）对妊娠期高血压胎盘滋养细胞增殖、凋亡及磷酸肌醇3激酶/蛋白激酶B（phosphoinositide-3 kinase/protein kinase B，PI3K/Akt）通路的影响。 方法 购买人胎盘滋养细胞，使用100 μmol/L N-硝基-L-精氨酸甲酯诱导胎盘滋养细胞模拟妊娠期高血压微环境，分为细胞空白组（N-硝基-L-精氨酸甲酯诱导胎盘滋养细胞）、过表达组（N-硝基-L-精氨酸甲酯诱导胎盘滋养细胞后做miR-26b过表达质粒转染）、沉默组（N-硝基-L-精氨酸甲酯诱导胎盘滋养细胞后做miR-26b沉默质粒转染）。检测3组细胞增殖、细胞凋亡、细胞PI3K/Akt通路蛋白表达情况。 结果 与空白组相比，过表达组miR-26b表达量升高，沉默组miR-26b表达量降低（P＜0.05），说明miR-26b转染成功。过表达组24 h、48 h、72 h细胞增殖率逐渐降低，沉默组逐渐升高，3组在组间、时点间、组间·时点间差异均有统计学意义（P＜0.05）。与空白组相比，过表达组PI3K、p-PI3K、Akt、p-Akt、Bcl-2蛋白表达量降低，Bax蛋白表达量升高（P＜0.05）；与空白组相比，沉默组PI3K、p-PI3K、Akt、p-Akt、Bcl-2蛋白表达量升高，Bax蛋白表达量降低（P＜0.05）；与过表达组相比，沉默组PI3K、p-PI3K、Akt、p-Akt、Bcl-2蛋白表达量升高，Bax蛋白表达量降低（P＜0.05）。 结论 沉默miR-26b可抑制妊娠期高血压胎盘滋养细胞凋亡、促进增殖，其作用机制可能与PI3K/Akt通路被激活相关。

The effect of silencing miR-26b viaPI3K/Akt pathway on proliferation and apoptosis of placental trophoblastic cells in patients with pregnancy-induced hypertension

Objective To analyze the effects of silencing micro RNA-26b(miR-26b) on proliferationand apoptosis of placental trophoblastic cells and PI3K/Akt pathway in patients with pregnancy-induced hypertension(PIH).Methods Human placental trophoblastic cells were purchased, and induced by 100 μmol/L N-nitro-L-arginine methyl ester to simulate the microenvironment of PIH. The blank group(N-nitro-L-arginine methyl ester induced placental trophoblastic cells), the overexpression group(N-nitro-L-arginine methyl ester induced placental trophoblastic cells which was transfected with miR-26b for overexpressionplasmid transfection), and the silence group(N-nitro-L-arginine methyl ester-induced placental trophoblastic cells that were silenced by miR-26b for plasmid transfection). Cell proliferation, apoptosis and PI3K/Akt pathway protein expression were detected.Results Compared with the blank group, the expression of miR-26b was increased in the overexpression group and decreased in the silencing group(P＜0.05), indicating that miR-26b was successfully transfected. The cell proliferation rate at 24 h, 48 h and 72 h in the overexpression group was gradually decreased, while that of the silence group was gradually increased, and the differences between groups, time points and time points between groups were statistically significant in three groups(P＜0.05).Compared with the blank group, the expression of PI3K, p-PI3K, Akt, p-Akt and Bcl-2 protein was decreased and the expression of Bax protein was increased in the overexpression group(P＜0.05). Compared with the blank group, the expression of PI3K, p-PI3K, Akt, p-Akt and Bcl-2 protein was increased and the expression of Bax protein was decreased in the silencing group(P＜0.05). Compared with the overexpression group, the expression of PI3K, p-PI3K, Akt, p-Akt and Bcl-2 protein was increased and the expression of Bax protein was decreased in the silencing group(P＜0.05).Conclusion Silencing miR-26b can inhibit apoptosis and promote proliferation of placental trophoblastic cells in patients with PIH, and its underlying mechanism may be related to the activation of PI3K/Akt pathway.