[1]刘龙梅,石懿玉,杨 霞,等.急性缺氧诱导小鼠心肌细胞微小RNA-34a升高和凋亡实验研究[J].陕西医学杂志,2023,52(10):1295-1298,1303.[doi:DOI:10.3969/j.issn.1000-7377.2023.10.003]
　LIU Longmei,SHI Yiyu,YANG Xia,et al.Experimental study of microRNA-34a elevation and apoptosis in mouse cardiomyocytes induced by acute hypoxia[J].,2023,52(10):1295-1298,1303.[doi:DOI:10.3969/j.issn.1000-7377.2023.10.003]
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急性缺氧诱导小鼠心肌细胞微小RNA-34a升高和凋亡实验研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
52
期数:
2023年10期
页码:
1295-1298,1303
栏目:
基础研究
出版日期:
2023-10-05

文章信息/Info

Title:
Experimental study of microRNA-34a elevation and apoptosis in mouse cardiomyocytes induced by acute hypoxia
作者:
刘龙梅; 石懿玉; 杨 霞; 介 希; 连婷婷; 王仲朝; 韩学斌
(山西省心血管病医院/研究所 山西医科大学附属心血管病医院,山西 太原 030024)
Author(s):
LIU Longmei; SHI Yiyu; YANG Xia; JIE Xi; LIAN Tingting; WANG Zhongchao; HAN Xuebin
(Shanxi Province Cardiovascular Hospital/Institute,Taiyuan 030024,China)
关键词:
miR-34a;  纳米颗粒;  PNUTS;  心肌细胞凋亡;  急性缺氧;  心肌梗死
Keywords:
miR-34a;  Nanoparticles;  PNUTS;  Cardiomyocyte apoptosis;  Acute hypoxia;  Myocardial infarction
分类号:
R 542.22
DOI:
DOI:10.3969/j.issn.1000-7377.2023.10.003
文献标志码:
A
摘要:
目的:探讨急性缺氧对心肌细胞miR-34a表达、蛋白磷酸酶1核靶向亚基(PNUTS)蛋白和凋亡的影响。方法:原代培养小鼠乳鼠心肌细胞,缺氧24 h造模,使用antimiR-34a纳米颗粒干预。将其随机分为三组:对照组、缺氧组、缺氧+antimiR-34a纳米颗粒组。采用实时荧光定量聚合酶链反应(qRT-PCR)测miR-34a表达,Western blot检测PNUTS蛋白表达,流式细胞术测凋亡率。结果:与对照组相比,缺氧24 h后miR-34a表达明显增高(P<0.05),PNUTS水平降低(P<0.05),凋亡率升高(P<0.05); 与缺氧组相比,缺氧+antimiR-34a纳米颗粒组的miR-34a表达下降(P<0.05),PNUTS水平升高(P<0.05),凋亡率下降(P<0.05)。结论:急性缺氧上调小鼠心肌细胞miR-34a基因表达,下调其下游PNUTS蛋白表达,同时上调凋亡率; antimiR-34a纳米颗粒抑制急性缺氧诱导的小鼠心肌细胞miR-34a升高,PNUTS降低以及细胞凋亡。
Abstract:
Objective:To investigate the effects of acute hypoxia on miR-34a expression,PNUTS protein and apoptosis in mouse cardiomyocytes.Methods:Primary cultured mouse mammary heart myocytes were cultured and modeled with hypoxia for 24 hours and intervened with antimiR-34a nanoparticles.They were randomly divided into three groups:control group,hypoxia group,and hypoxia+antimiR-34a nanoparticles group.The expression of miR-34a was measured by qRT-PCR,and the expression of PNUTS protein was detected by Western blot.Apoptosis rate was measured by flow cytometry.Results:Compared with the control group,miR-34a expression was significantly increased(P<0.05),PNUTS level was decreased(P<0.05),and apoptosis rate was increased(P<0.05)after 24 hours of hypoxia.Compared with the hypoxia group,miR-34a expression was decreased(P<0.05),PNUTS level was increased(P<0.05)in the hypoxia+antimiR-34a nanoparticles group,and apoptosis rate was decreased(P<0.05).Conclusion:Acute hypoxia up-regulates miR-34a expression,down-regulates its downstream PNUTS protein expression,and increases apoptosis rate in mouse cardiomyocytes.AntimiR-34a nanoparticles inhibit the increase of miR-34a,the decrease of PNUTS and the apoptosis of mouse cardiomyocytes induced by acute hypoxia.

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备注/Memo

备注/Memo:
基金项目:山西省重点研发计划(国际科技合作)项目(201803D421052); 山西省心血管病医院科研激励计划项目(XYS20170204)
更新日期/Last Update: 2023-10-07