首页|环状RNA circ-SLAIN2在急性心肌炎患者血清中表达及对心肌细胞活性的影响

环状RNA circ-SLAIN2在急性心肌炎患者血清中表达及对心肌细胞活性的影响

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目的:观察环状RNA(circRNA)circ-SLAIN2在急性心肌炎患者血清中的表达,探讨circ-SLAIN2对心肌细胞增殖和凋亡的影响及作用机制。方法:收集35例急性心肌炎患者血清标本,另选取35例体检健康者为对照,采用实时定量聚合酶链反应(qRT-PCR)检测血清中circ-SLAIN2表达量。选取人心肌细胞系HCM,分别感染空载慢病毒(对照组)或载有circ-SLAIN2序列的慢病毒(circ-SLAIN2组)。qRT-PCR检测circ-SLAIN2过表达效率。分别采用脂多糖诱导心肌炎,采用细胞计数试剂盒8(CCK-8)法和流式细胞术检测过表达circ-SLAIN2对人心肌细胞增殖和凋亡的影响。LncBase v。2、Linc2GO、LNCipedia、miRcode在线数据库和双荧光素酶报告基因实验分析circ-SLAIN2和微小RNA-429(miR-429)的靶向关系。qRT-PCR检测miR-429表达水平。蛋白质印迹(Western blot)法检测丝裂原活化蛋白激酶p38(p38MAPK)/核因子κB(NF-κB)信号通路蛋白和凋亡相关蛋白的表达水平。结果:急性心肌炎患者血清中circ-SLAIN2表达较体检健康者显著降低(P<0。01)。与对照组比较,circ-SLAIN2组HCM细胞中circ-SLAIN2表达显著上升(P<0。01)。经过脂多糖处理36 h后,circ-SLAIN2组HCM细胞增殖吸光度明显高于对照组(P<0。01),circ-SLAIN2组HCM细胞凋亡率明显低于对照组(P<0。01)。circ-SLAIN2能够靶向结合miR-429。与对照组比较,circ-SLAIN2组HCM细胞中miR-429表达显著降低(P<0。01),p38MAPK/NF-κB信号通路蛋白表达显著降低(P<0。01),细胞凋亡蛋白Bcl-2相关X蛋白(Bax)、Bcl-2相关K蛋白(Bak)表达量降低(均P<0。01)。结论:circ-SLAIN2在急性心肌炎患者血清中低表达,过表达circ-SLAIN2通过负向调节miR-429表达,增强心肌细胞的活性并抑制细胞的凋亡。
Expression of circular RNA circ-SLAIN2 in serum of patients with acute myocarditis and its effect on myocardial cell activity
Objective:To observe the expression of circular RNA(circRNA)circ-SLAIN2 in serum of patients with acute myocarditis,and to explore the effect of circ-SLAIN2 on myocardial cell proliferation and apoptosis and its mechanism.Methods:Serum samples from 35 patients with acute myocarditis treated in the Department of Cardiovas-cular Medicine,Jingmen People's Hospital from July 2020 to May 2023 were collected,and 35 healthy individuals were selected as controls.The expression of circ-SLAIN2 in serum was detected by quantitative real-time polymerase chain reaction(qRT-PCR).The human cardiomyocyte cell line HCM was selected and infected with empty lentivirus(Control group)or lentivirus loaded with circ-SLAIN2 sequence(circ-SLAIN2 group).The overexpression efficiency of circ-SLAIN2 was detected by qRT-PCR.Myocarditis was induced by lipopolysaccharide,and the effects of circ-SLAIN2 overexpression on the proliferation and apoptosis of human cardiomyocytes were detected by Cell Counting Kit-8(CCK-8)assay and flow cytometry.The LncBase v.2,Linc2GO,LNCipedia,miRcode online database and dual-luciferase reporter gene experiments were used to analyze the targeting relationship between circ-SLAIN2 and miR-429.The expression level of miR-429 was detected by qRT-PCR.Western blot was used to detect the expression lev-els of Mitogen-activated protein kinase p38(p38MAPK)/nuclear factor-kappa B(NF-κB)signaling pathway pro-teins and apoptosis-related proteins.Results:The expression of circ-SLAIN2 in serum of patients with acute myocar-ditis was significantly lower than that of healthy subjects(P<0.01).Compared with the control group,the expres-sion of circ-SLAIN2 in HCM cells in the circ-SLAIN2 group was significantly increased(P<0.01).After lipopo-lysaccharide treatment for 36 h,the absorbance of HCM cell proliferation in circ-SLAIN2 group was significantly higher than that in Control group(P<0.01),and the apoptosis rate of HCM cells in circ-SLAIN2 group was signifi-cantly lower than that in Control group(P<0.01).circ-SLAIN2 can target and bind miR-429.Compared with the control group,the expression of miR-429 in HCM cells in the circ-SLAIN2 group was significantly decreased(P<0.01),the expression of p38MAPK/NF-κB signaling pathway proteins was significantly decreased(P<0.01),and the expression of apoptosis proteins Bcl-2 associated X protein(Bax),Bcl-2 associated K protein(Bak)was decreased(all P<0.01).Conclusion:circ-SLAIN2 is lowly expressed in the serum of patients with acute myocarditis,and over-expression of circ-SLAIN2 negatively regulates the expression of miR-429,enhances the activity of cardiomyocytes and inhibits cell apoptosis.

Acute myocarditisCircular RNACirc-SLAIN2MiR-429Cell proliferationCell apoptosis

朱丽、伍仙凤、夏玮、刘玲玲、徐薇

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荆门市人民医院 荆楚理工学院附属中心医院心血管内科,湖北荆门 448000

荆门市人民医院 荆楚理工学院附属中心医院老年科,湖北荆门 448000

苏州大学附属第二医院心血管内科,江苏苏州 215004

急性心肌炎 环状RNA circ-SLAIN2 微小RNA-429 细胞增殖 细胞凋亡

2025

陕西医学杂志
陕西省中医药研究院

陕西医学杂志

影响因子:1.011
ISSN:1000-7377
年,卷(期):2025.54(1)