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首页> 外文期刊>Cellular Physiology and Biochemistry >Protective Effects of MicroRNA-126 on Human Cardiac Microvascular Endothelial Cells Against Hypoxia/Reoxygenation-Induced Injury and Inflammatory Response by Activating PI3K/Akt/eNOS Signaling Pathway
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Protective Effects of MicroRNA-126 on Human Cardiac Microvascular Endothelial Cells Against Hypoxia/Reoxygenation-Induced Injury and Inflammatory Response by Activating PI3K/Akt/eNOS Signaling Pathway

机译：MicroRNA-126通过激活PI3K / Akt / eNOS信号通路对人心脏微血管内皮细胞的抗缺氧/复氧性损伤和炎症反应的保护作用

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>Objective: This study explored the protective effects of the microRNA-126 (miR-126)-mediated PI3K/Akt/eNOS signaling pathway on human cardiac microvascular endothelial cells (HCMECs) against hypoxia/reoxygenation (H/R)-induced injury and the inflammatory response. Methods: Untreated HCMECs were selected for the control group. After H/R treatment and cell transfection, the HCMECs were assigned to the H/R, miR-126 mimic, mimic-negative control (NC), miR-126 inhibitor, inhibitor-NC, wortmannin (an inhibitor of PI3K) and miR-126 mimic + wortmannin groups. Super oxide dismutase (SOD), nitric oxide (NO), vascular endothelial growth factor (VEGF) and reactive oxygen species (ROS) were measured utilizing commercial kits. Quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to detect miR-126 expression and the mRNA and protein expression of inflammatory factors. Western blotting was used to determine the expression of key members in the PI3K/Akt/eNOS signaling pathway. ACCK-8 assay and flow cytometry were employed to examine cell proliferation and apoptosis, respectively. The angiogenic ability in each group was detected by the lumen formation test. Results: Compared to the control group, p/t-PI3K, p/t-Akt and p/t-eNOS expression, NO, VEGF and SOD levels, cell proliferation and in vitro lumen formation ability were decreased, while the ROS content, interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-?± expression and cell apoptosis were significantly increased in the H/R, mimic-NC, miR-126 inhibitor, inhibitor-NC, wortmannin and miR-126 mimic + wortmannin groups. Additionally, in comparison with the H/R group, the miR-126 mimic group had elevated p/t-PI3K, p/t-Akt and p/t-eNOS expression, increased NO, VEGF and SOD contents, and strengthened cell proliferation and lumen formation abilities but also exhibited decreased ROS content, reduced IL-6, IL-10 and TNF-?± expressions, and weakened cell apoptosis, while the miR-126 inhibitor and wortmannin group exhibited the opposite results. Furthermore, decreased p/t-PI3K, p/t-Akt and p/t-eNOS expressions, decreased NO, VEGF and SOD contents, cell proliferation and lumen formation abilities, as well as increased ROS content, increased IL-6, IL-10 and TNF-?± expression, and increased cell apoptosis were observed in the miR-126 mimic + wortmannin group compared to themiR-126 mimic group. Conclusions: These findings indicated that miR-126 protects HCMECs from H/R-induced injury and inflammatory response by activating the PI3K/Akt/ eNOS signaling pathway.
机译：> 目的： 本研究探讨了microRNA-126（miR-126）介导的PI3K / Akt / eNOS信号通路对人心脏微血管内皮细胞的保护作用。 （HCMEC）对抗缺氧/复氧（H / R）诱导的损伤和炎症反应。 方法： 选择未经治疗的HCMEC作为对照组。经过H / R治疗和细胞转染后，将HCMECs分配到H / R，miR-126模拟物，模拟阴性对照（NC），miR-126抑制剂，抑制剂NC，渥曼青霉素（PI3K抑制剂）和miR -126个模拟物+渥曼青霉素组。使用商业试剂盒测量了超氧化物歧化酶（SOD），一氧化氮（NO），血管内皮生长因子（VEGF）和活性氧（ROS）。进行实时定量聚合酶链反应（qRT-PCR）和酶联免疫吸附测定（ELISA），以检测miR-126表达以及炎症因子的mRNA和蛋白质表达。 Western印迹用于确定PI3K / Akt / eNOS信号通路中关键成员的表达。使用ACCK-8测定法和流式细胞术分别检查细胞增殖和凋亡。通过管腔形成试验检测每组中的血管生成能力。 结果： 与对照组相比，p / t-PI3K，p / t-Akt和p / t-eNOS表达，NO，VEGF和SOD水平，细胞增殖小鼠体内和体外的管腔形成能力降低，而ROS的含量，白介素（IL）-6，IL-10和肿瘤坏死因子（TNF）-α±的表达和细胞凋亡均明显增加。 H / R，mimic-NC，miR-126抑制剂，抑制剂NC，渥曼青霉素和miR-126模仿+渥曼青霉素组。此外，与H / R组相比，miR-126模拟组的p / t-PI3K，p / t-Akt和p / t-eNOS表达升高，NO，VEGF和SOD含量增加，并增强了细胞增殖但是，miR-126抑制剂和渥曼青霉素组却表现出相反的结果，但其内腔形成能力和管腔形成能力降低，但ROS含量降低，IL-6，IL-10和TNF-α±表达降低，细胞凋亡减弱。此外，p / t-PI3K，p / t-Akt和p / t-eNOS表达降低，NO，VEGF和SOD含量降低，细胞增殖和管腔形成能力降低，ROS含量升高，IL-6，IL升高与miR-126模仿组相比，miR-126模仿+渥曼青霉素组观察到-10和TNF-α±表达，并增加细胞凋亡。 结论： 这些发现表明，miR-126通过激活PI3K / Akt / eNOS信号通路，保护HCMEC免受H / R诱导的损伤和炎症反应。

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