[1]袁孝伟 宣学习 周芃 刘魁智 王豪 朱自强.lncRNA SNHG6通过调节miR-26a-5p/CTGF轴影响心房颤动大鼠心肌纤维化的作用机制?/html>[J].心血管病学进展,2025,(2):186.[doi:10.16806/j.cnki.issn.1004-3934.202.02.018]
　YUAN Xiaowei,XUAN Xuexi,ZHOU Peng,et al.The Mechanism of lncRNA SNHG6 Affecting Myocardial Fibrosis in Rats with Atrial Fibrillation by Regulating the miR-26a-5p/CTGF Axis[J].Advances in Cardiovascular Diseases,2025,(2):186.[doi:10.16806/j.cnki.issn.1004-3934.202.02.018]
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lncRNA SNHG6通过调节miR-26a-5p/CTGF轴影响心房颤动大鼠心肌纤维化的作用机制?/html>()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2025年2期
页码:
186
栏目:
论著
出版日期:
2025-02-25

文章信息/Info

Title:
The Mechanism of lncRNA SNHG6 Affecting Myocardial Fibrosis in Rats with Atrial Fibrillation by Regulating the miR-26a-5p/CTGF Axis
作者:
102;  102); font-family: Arial;  Verdana;  sans-serif; font-size: 12px; background-color: rgb(255;  255;  255);">袁孝伟 宣学习 周芃 刘魁智 王豪 朱自强
（郑州市第七人民医院心血管内科，河南 郑州 450016）
Author(s):
YUAN Xiaowei; XUAN Xuexi; ZHOU Peng; LIU Kuizhi; WANG Hao; ZHU Ziqiang
(Department of Cardiovascular Medicine,The 7th People’s Hospital of Zhengzhou,Zhengzhou 450016,Henan,China)
关键词:
非编码RNA; 小核仁RNA宿主基因6; miR-26a-5p; 结缔组织生长因子; 心房颤动; 心肌纤维化
Keywords:
Long non-coding RNA;  Small nucleolar RNA host gene 6;  miR-26a-5p;  Connective tissue growth factor;  Atrial fibrillation;  Myocardial fibrosis
DOI:
10.16806/j.cnki.issn.1004-3934.202.02.018
摘要:
目的 探讨长非编码RNA（lncRNA）小核仁RNA宿主基因6（SNHG6）通过调节miR-26a-5p/结缔组织生长因子（CTGF）轴对心房颤动（AF）大鼠心肌纤维化的影响。方法 验证lncRNA SNHG6与miR-26a-5p、miR-26a-5p与CTGF的关系构建AF模型大鼠，将造模成功60只大鼠随机分为AF组、sh-NC组、sh-lncRNA SNHG6组、sh-lncRNA SNHG6+anti-miR-NC组、sh-lncRNA SNHG6+anti-miR-26a-5p组，每组12只。另取12只大鼠作为正常组。检测大鼠AF持续时间、AF发生率变化；qRT-PCR检测心房组织中lncRNA SNHG6、miR-26a-5p水平及CTGF mRNA水平；超氧化物阴离子荧光探针（DHE）染色检测心房组织中活性氧（ROS）平均荧光强度；试剂盒检测心房组织中丙二醛（MDA）、超氧化物歧化酶（SOD）水平；Masson染色心房组织中心肌纤维化；检测心房组织中胶原蛋白I（Collagen I）、基质金属蛋白酶9（MMP-9）、转化生长因子β1（TGF-β1）、CTGF蛋白。结果 靶向调节miR-26a-5p/CTGF轴与AF组、sh-NC组比较，sh-lncRNA SNHG6组心房组织呈蓝染的纤维化面积减少，AF持续时间、AF发生率、心房组织中 SNHG6水平、CTGF mRNA水平、ROS平均荧光强度、MDA水平及Collagen I、MMP-9、TGF-β1、CTGF蛋白降低，心房组织中miR-26a-5p水平、SOD水平升高（P＜0.05）；anti-miR-26a-5p逆转了沉默 SNHG6对AF大鼠心肌纤维化的改善作用。结论 沉默 SNHG6可能通过调控miR-26a-5p/CTGF轴抑制氧化应激进而改善AF大鼠心肌纤维化。
Abstract:
Objective To investigate the effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) on myocardial fibrosis in rats with atrial fibrillation (AF) by regulating the miR-26a-5p/connective tissue growth factor (CTGF) axis. Methods The relationship between lncRNA SNHG6 and miR-26a-5p,between miR-26a-5p and CTGF was validated. The AF model rats were constructed,and the 60 successfully constructed rats were randomly divided into AF group,sh-NC group,sh-lncRNA SNHG6 group,sh-lncRNA SNHG6+anti-miR-NC group,and sh-lncRNA SNHG6+anti-miR-26a-5p group,with 12 rats in each group. Another 12 rats were selected as the normal group. The duration and incidence of AF in rats were detected. QRT-PCR was applied to detect the levels of lncRNA SNHG6,miR-26a-5p,and CTGF mRNA in atrial tissue. Dihydroethidium (DHE) staining was applied to detect the average fluorescence intensity of reactive oxygen species (ROS) in atrial tissue. The reagent kits were applied to detect levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in atrial tissue. Masson staining was applied to detect central muscle fibrosis in atrial tissue. Western blot was applied to detect Collagen I,matrix metalloproteinase-9 (MMP-9),transforming growth factor-β1 (TGF-β1),and CTGF proteins in atrial tissue. Results lncRNA SNHG6 targeted and regulated the miR-26a-5p/CTGF axis. Compared with the AF group and sh-NC group,the atrial tissue in the sh-lncRNA SNHG6 group showed a reduction in fibrotic area with blue staining,the duration of AF,incidence of AF,levels of lncRNA SNHG6,CTGF mRNA,ROS average fluorescence intensity,level of MDA,and the levels of Collagen I,MMP-9,TGF-β1,and CTGF proteins in atrial tissue decreased,the levels of miR-26a-5p and SOD in atrial tissue increased (P<0.05). anti-miR-26a-5p reversed the improvement effect of silencing lncRNA SNHG6 on myocardial fibrosis in AF rats. Conclusion Silencing lncRNA SNHG6 may inhibit oxidative stress by regulating the miR-26a-5p/CTGF axis,thereby improving myocardial fibrosis in AF rats

参考文献/References:

[1] Hao H,Yan S,Zhao X,et al. Atrial myocyte-derived exosomal microRNA contributes to atrial fibrosis in atrial fibrillation[J]. J Transl Med,2022,20(1):407-422.
[2] Deng W,Zhang Y,Fang P,et al. Silencing lncRNA Snhg6 mitigates bleomycin-induced pulmonary fibrosis in mice via miR-26a-5p/TGF-β1-smads axis[J]. Environ Toxicol,2022,37(10):2375-2387.
[3] 何涛丁安周文杰等. miR-26a-5p下调DNMT3A表达抑制心肌成纤维细胞活化增殖的机制研究[J]. 中国循证心血管医学杂志2020,12(10):1179-1184.
[4] 谭珍妮吕春美邹海林. LncRNA NEAT1调节miR-27b-3p、SP1对心房颤动大鼠心肌纤维化的影响[J]. 中国动脉硬化杂志2024,1(1):1-16.
[5] 袁孝伟赵育洁陈丰毅等. 穿心莲内酯调节YAP/TAZ信号通路对心房颤动大鼠心肌纤维化的影响[J]. 中药材2023,46(10):2585-2590.
[6] Xu L,Fan Y,Wu L,et al. Exosomes from bone marrow mesenchymal stem cells with overexpressed nrf2 inhibit cardiac fibrosis in rats with atrial fibrillation[J]. Cardiovasc Ther,2022,2022:2687807.
[7] Wang D,Wang X,Yang T,et al. Long non-coding rna dancr affects myocardial fibrosis in atrial fibrillation mice via the microrna-146b-5p/Smad5 axis[J]. Acta Cardiol Sin,2023,39(6):841-853.
[8] 张梦伟赵忠帅杨林等. SNHG6靶向miR-101/TGFBR1促进AMI小鼠左心室心肌纤维化[J]. 中南医学科学杂志2023,51(5):640-644.
[9] 尤其郭辉. LncRNA SNHG6调控miR-335-3p/PDCD4途径对缺氧复氧诱导的心肌细胞损伤的影响[J]. 心电与循环2021,40(4):355-361.
[10] Quah JX,Dharmaprani D,Tiver K,et al. Atrial fibrosis and substrate based characterization in atrial fibrillation: Time to move forwards[J]. J Cardiovasc Electrophysiol,2021,32(4):1147-1160.
[11] Zhu J,Zhu N,Xu J. MiR-101a-3p overexpression prevents acetylcholine-CaCl2-induced atrial fibrillation in rats via reduction of atrial tissue fibrosis,involving inhibition of EZH2[J]. Mol Med Rep,2021,24(4):740-749.
[12] Liu X,Zhao L,Gao Y,et al. AMP-activated protein kinase inhibition in fibro-adipogenic progenitors impairs muscle regeneration and increases fibrosis[J]. J Cachexia Sarcopenia Muscle,2023,14(1):479-492.
[13] Han X,Wang S,Yong Z,et al. Effect of miR-499-5p/SOX6 axis on atrial fibrosis in rats with atrial fibrillation[J]. Open Med (Wars),2023,18(1):20230654.
[14] Leventopoulos G,Koros R,Travlos C,et al. Mechanisms of atrial fibrillation: how our knowledge affects clinical practice[J]. Life (Basel),2023,13(6):1260-1277.
[15] Koizumi T,Watanabe M,Yokota T,et al. Empagliflozin suppresses mitochondrial reactive oxygen species generation and mitigates the inducibility of atrial fibrillation in diabetic rats[J]. Front Cardiovasc Med,2023,10:1005408.
[16] Luo Y,Xu H,Yang Z,et al. Long non-coding RNA MALAT1 silencing elevates microRNA-26a-5p to ameliorate myocardial injury in sepsis by reducing regulator of calcineurin 2[J]. Arch Biochem Biophys,2022,715:109047.
[17] Shi H,Li H,Zhang F,et al. MiR-26a-5p alleviates cardiac hypertrophy and dysfunction via targeting ADAM17[J]. Cell Biol Int,2021,45(11):2357-2367.
[18] Liu N,Zhen Z,Xiong X,et al. Aerobic exercise protects MI heart through miR-133a-3p downregulation of connective tissue growth factor[J]. PLoS One,2024,19(1):e0296430.
[19] 石晶晶孟昊寿鑫甜等. 芪珀生脉颗粒通过调节PI3K/SGK1信号通路改善心房颤动大鼠心房肌纤维化[J]. 北京中医药2022,41(10):1079-1083.
[20] 霍雨佳,阳远舟,邹成丽,等. 汉黄芩素调节Hippo/YAP信号通路对慢性心力衰竭大鼠心肌纤维化的影响[J]. 中西医结合心脑血管病杂志,2024,22(15):2740-2745.

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备注/Memo

备注/Memo:
收稿日期：2024-08-27基金项目：2023年度河南省医学科技攻关计划联合共建项目（LHGJ20230738）
更新日期/Last Update: 2025-03-11