基础医学与临床 ›› 2021, Vol. 41 ›› Issue (7): 995-1000.

• 研究论文 • 上一篇    下一篇

miR-193a-3p抑制高糖诱导人视网膜血管内皮细胞凋亡

秦建民1,张来香2,魏振英3   

  1. 1. 青岛市第八人民医院
    2. 青岛市中心医院
    3. 青岛市妇女儿童医院
  • 收稿日期:2020-06-16 修回日期:2020-11-19 出版日期:2021-07-05 发布日期:2021-06-17
  • 通讯作者: 秦建民 E-mail:tx9h45@163.com

miR-193a-3p inhibits hyperglycose-induced apoptosis of human retinal vascular endothelial cells

  • Received:2020-06-16 Revised:2020-11-19 Online:2021-07-05 Published:2021-06-17

摘要: 目的 探讨miR-193a-3p对高糖诱导的人视网膜血管内皮细胞(HRECs)凋亡的影响和分子机制。方法 体外培养HRECs细胞,建立高糖(葡萄糖浓度为30 mmol/L)HRECs细胞模型。设置对照组、模型组、anti-miR-NC、ani-miR-193a-3p组、模型+miR-NC组、模型+miR-193a-3p组、模型+LY294002。RT-qPCR检测miR-193a-3p的表达水平;Western blot检测活化的含半胱氨酸的天冬氨酸蛋白水解酶3(C-caspase-3)、B细胞淋巴瘤/白血病-2(Bcl-2)、磷酸化的磷酸肌醇3激酶(p-PI3K)和磷酸化的蛋白激酶B(p-AKT)的表达水平;流式细胞仪检测细胞凋亡。结果 模型组与对照组比较,miR-193a-3p、Bcl-2表达显著降低,凋亡率、C-caspase-3、p-PI3K和p-AKT表达显著升高(P<0.05)。低表达miR-193a-3p促进C-caspase-3、p-PI3K和p-AKT表达,抑制Bcl-2表达,促进细胞凋亡(P <0.05)。高表达miR-193a-3p可减轻高糖处理对HRECs凋亡、C-caspase-3和Bcl-2表达的影响(P <0.05)。抑制PI3K/AKT信号通路可减轻高糖处理对HRECs凋亡、C-caspase-3和Bcl-2表达的影响(P <0.05)。结论 miR-193a-3p可能通过调控PI3K/AKT信号通路抑制高糖诱导人视网膜血管内皮细胞凋亡。

关键词: miR-193a-3p, PI3K/AKT信号通路, 人视网膜血管内皮细胞, 高糖, 凋亡

Abstract: Objective To investigate the effect of miR-193a-3p on apoptosis induced by high glucose in human retinal vascular endothelial cells (HRECs) and its molecular mechanism. Methods HRECs cells were cultured in vitro to establish a high glucose (30 mmol/L glucose concentration) cell model. HRECs were divided into Control group, model group, anti-miR-NC group, anti-miR-193a-3p group, model+miR-NC group, model+miR-193a-3p group, and model +LY294002 group. RT-qPCR was used to detect the expression level of miR-193a-3p; Western blot was used to detect the expression levels of cleaved caspase 3 (C-caspase-3), B cell lymphoma/leukemia-2 (Bcl-2), phosphorylated phosphoinositide 3 kinase (p-PI3K) and phosphorylated protein kinase B (p-AKT); flow cytometry was used to detect cell apoptosis. Results Compared with the control group, the expressions of miR-193a-3p and Bcl-2 in the model group were significantly decreased, whereas apoptosis rate, and the expressions of C-Caspase-3, P-PI3K and P-Akt were significantly increased (P<0.05). Low expression of miR-193a-3p promotes C-caspase-3, p-PI3K and p-AKT expression, inhibits Bcl-2 expression, and promotes cell apoptosis (P <0.05). High expression of miR-193a-3p can significantly reduce the effect of high glucose treatment on the apoptosis, C-caspase-3 and Bcl-2 expression of HRECs (P<0.05). Inhibition of PI3K/AKT signaling pathway reverses the effect of high glucose treatment the apoptosis, C-caspase-3 and Bcl-2 expression of HRECs (P<0.05). Conclusions miR-193a-3p may inhibit high glucose-induced apoptosis of human retinal vascular endothelial cells by regulating PI3K/AKT signaling pathway.

Key words: miR-193a-3p, PI3K/AKT signaling pathway, human retinal vascular endothelial cells, high glucose, apoptosis