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Protective effects of ginsenoside Rb1 on H2O2-induced oxidative injury in human endothelial cell line (EA.hy926) via miR-210.
International Journal of Immunopathology and Pharmacology ( IF 3.5 ) Pub Date : 2019-07-31 , DOI: 10.1177/2058738419866021
Fubao Jia 1 , Lei Mou 2 , Hanming Ge 3
Affiliation  

Ginsenoside Rb1 (Rb1) possesses a cardioprotective effect via mediating microRNAs (miRs), while it is unexplored whether miR-210 is regulated by Rb1 in response to oxidative stress. Human endothelial EA.hy926 cells were stimulated with H2O2 before Rb1 treatment. After transfection, cell viability, apoptosis, migration, and invasion assays were conducted. Western blot was applied to quantify protein. BCL2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3) and miR-210 were analyzed with quantitative reverse transcription polymerase chain reaction. Dual luciferase activity assay was performed. Rb1 elevated viability, migration, and invasion of H2O2-treated cells. H2O2-induced apoptosis was moderated by Rb1. miR-210 was augmented in H2O2-treated cells after Rb1 stimulation. miR-210 inhibitor abolished the positive effects of Rb1. BNIP3 was negatively modulated by miR-210 and implicated in modulating viability, apoptosis, and migration and invasion. In addition, BNIP3 modulated phosphorylation of regulators. Rb1 repressed oxidative injury via elevating miR-210. miR-210 negatively mediated BNIP3, which participated in oxidative damage via regulating mammalian targets of rapamycin (mTOR) and nuclear factor-κB (NF-κB).

中文翻译:

人参皂苷 Rb1 通过 miR-210 对 H2O2 诱导的人内皮细胞系 (EA.hy926) 氧化损伤的保护作用。

人参皂苷 Rb1 (Rb1) 通过介导 microRNA (miR) 具有心脏保护作用,而 miR-210 是否受 Rb1 调节以响应氧化应激尚不清楚。在 Rb1 处理之前,用 H2O2 刺激人内皮 EA.hy926 细胞。转染后,进行细胞活力、细胞凋亡、迁移和侵袭测定。应用蛋白质印迹来定量蛋白质。BCL2/腺病毒 E1B 19-kDa 相互作用蛋白 3 (BNIP3) 和 miR-210 用定量逆转录聚合酶链反应进行分析。进行双荧光素酶活性测定。Rb1 提高了 H2O2 处理细胞的活力、迁移和侵袭。H2O2 诱导的细胞凋亡受 Rb1 的调节。在 Rb1 刺激后,miR-210 在 H2O2 处理的细胞中增加。miR-210 抑制剂消除了 Rb1 的积极作用。BNIP3 受到 miR-210 的负调节,并参与调节活力、细胞凋亡、迁移和侵袭。此外,BNIP3 调节调节剂的磷酸化。Rb1 通过升高 miR-210 抑制氧化损伤。miR-210 负介导 BNIP3,BNIP3 通过调节哺乳动物雷帕霉素靶标 (mTOR) 和核因子-κB (NF-κB) 参与氧化损伤。
更新日期:2019-11-01
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