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武国利,马竞.miR-376b-3p通过靶向FGF21加重缺氧复氧心肌细胞的损伤[J].中国动脉硬化杂志,2020,(10):875~881
miR-376b-3p通过靶向FGF21加重缺氧复氧心肌细胞的损伤
Mechanism of miR-376b-3p promoting the injury of hypoxia reoxygenation myocardial cells by targeting FGF21
投稿时间:2019-11-11  修订日期:2019-12-19
DOI:
中文关键词:  miR-376b-3p  成纤维细胞生长因子21  缺氧复氧  心肌细胞
英文关键词:miR-376b-3p  FGF21  hypoxia reoxygenation  cardiomyocytes
基金项目:河北省保定市科技计划项目(1951ZF058)
作者单位E-mail
武国利 保定市第一中心医院,河北省保定市 071000 e-mail为f0yyef@163.com,e-mail为2002.abc@163.com 
马竞 河北大学附属医院,河北省保定市 071000 e-mail为f0yyef@163.com,e-mail为2002.abc@163.com 
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中文摘要:
      目的 探讨miR-376b-3p对缺氧复氧(H/R)心肌细胞增殖、凋亡的影响及机制。方法 培养心肌细胞H9c2,缺氧复氧法体外模拟H/R细胞损伤,建立心肌细胞损伤模型。用流式细胞术、免疫印迹(Western blot)、酶联免疫吸附(ELISA)检测正常对照组、H/R组、anti-miR-NC组、anti-miR-376b-3p组、anti-miR-376b-3p+si-NC组、anti-miR-376b-3p+si-成纤维细胞生长因子21(FGF21)组细胞凋亡率、凋亡相关蛋白B淋巴细胞瘤2基因(Bcl-2)、Bcl-2相关X蛋白(Bax)表达和肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素17(IL-17)情况。双荧光素酶报告基因实验检测细胞的荧光活性。结果 成功建立缺氧复氧损伤的细胞模型;模型组细胞中miR-376b-3p表达显著升高,FGF21表达显著降低,并且抑制miR-376b-3p可以减轻损伤细胞的凋亡和TNF-α、IL-6、IL-17的含量,以及上调Bcl-2,下调Bax。此外,miR-376b-3p还可靶向FGF21 mRNA。抑制FGF21后,抑制miR-376b-3p对缺氧复氧损伤的H9c2细胞的保护作用被减弱。结论 miR-376b-3p可促进缺氧复氧心肌细胞的凋亡和炎性反应,其机制与靶向FGF21 mRNA相关。
英文摘要:
      Aim To investigate the effect and mechanism of miR-376b-3p on proliferation and apoptosis of hypoxia reoxygenation (H/R) cardiomyocytes. Methods Cultured cardiomyocyte H9c2, hypoxia-reoxygenation method was used to simulate hypoxia reoxygenation injury in vitro, and a model of myocardial cell injury was established. Flow cytometry, Western blot, enzyme-linked immunosorbent assay(ELISA) were used to detect the apoptosis rate, apoptosis-related B lymphoblastoma-2 gene(Bcl-2), Bcl-2 related X gene (Bax) protein expression and inflammatory factors secreted tumor necrosis factor α(TNF-α), interleukin-6 (IL-6) and interleukin-17 (IL-17) in normal control group, H/R group, anti-miR-NC group, anti-miR-376b-3p group, anti-miR-376b-3p+si-NC group, anti-miR-376b-3p+si-fibroblast growth factor 21(FGF21) group. The dual luciferase reporter gene assay was used to detect the fluorescence activity. Results A cell model of hypoxia reoxygenation injury was successfully established. miR-376b-3p mRNA expression was significantly increased, FGF21 mRNA and protein expression were significantly decreased in the model group. The cell apoptosis and inflammatory factor levels of TNF-α, IL-6, IL-17 were all inhibited, as well as up-regulation of Bcl-2 protein expression, down-regulation of Bax protein expression in inhibiting miR-376b-3p group. In addition, miR-376b-3p can also target FGF21 mRNA. After inhibiting FGF21,the protective effect of inhibiting miR-376b-3p on H9c2 cells damaged by hypoxia reoxygenation was weakened. Conclusion miR-376b-3p can promote the apoptosis and inflammatory response of hypoxia reoxygenation myocardial cells, and its mechanism may be related to targeting FGF21 mRNA.
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