Suppression of lncRNA OIP5-AS1 Attenuates Apoptosis and Inflammation, and Promotes Proliferation by Mediating miR-25-3p Expression in Lipopolysaccharide-Induced Myocardial Injury.

IF 2.6 4区医学 Q3 CELL BIOLOGY Analytical Cellular Pathology Pub Date : 2023-01-01 DOI:10.1155/2023/3154223

Jiaju Ma, Hebu Qian, Han Zou

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引用次数: 1

Abstract

Purpose: Long non-coding RNAs (LncRNAs) OIP5-AS1 and miR-25-3p play important roles in myocardial injury, whereas their roles in lipopolysaccharide (LPS)-induced myocardial injury remain unknown. The purpose of our study was to investigate the functional mechanisms of OIP5-AS1 and miR-25-3p in LPS-induced myocardial injury.

Methods: Rats and H9C2 cells were treated with LPS to establish the model of myocardial injury in vivo and in vitro, respectively. The expression levels of OIP5-AS1 and miR-25-3p were determined by quantitative reverse transcriptase-polymerase chain reaction. Enzyme-linked immunosorbent assay was performed to measure the serum levels of IL-6 and TNF-α. The relationship between OIP5-AS1 and miR-25-3p/NOX4 was determined by luciferase reporter assay and/or RNA immunoprecipitation assay. The apoptosis rate was detected by flow cytometry, and cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Western blot was performed to detect the protein levels of Bax, Bcl-2, caspase3, c-caspase3, NOX4, and p-NF-κB p65/NF-κB p65.

Results: OIP5-AS1 was up-regulated, and miR-25-3p was down-regulated in myocardial tissues of LPS-induced rats and LPS-treated H9C2 cells. Knockdown of OIP5-AS1 relieved the myocardial injury in LPS-induced rats. Knockdown of OIP5-AS1 also inhibited the inflammation and apoptosis of myocardial cells in vivo, which was subsequently confirmed by in vitro experiments. In addition, OIP5-AS1 targeted miR-25-3p. MiR-25-3p mimics reversed the effects of OIP5-AS1 overexpression on promoting cell apoptosis and inflammation and on inhibiting cell viability. Besides, miR-25-3p mimics blocked the NOX4/NF-κB signalling pathway in LPS-induced H9C2 cells.

Conclusion: Silencing of lncRNA OIP5-AS1 alleviated LPS-induced myocardial injury by regulating miR-25-3p.

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抑制lncRNA OIP5-AS1通过介导miR-25-3p在脂多糖诱导的心肌损伤中的表达，减轻细胞凋亡和炎症，促进细胞增殖。

目的:长链非编码rna (LncRNAs) OIP5-AS1和miR-25-3p在心肌损伤中发挥重要作用，而它们在脂多糖(LPS)诱导的心肌损伤中的作用尚不清楚。我们的研究目的是探讨OIP5-AS1和miR-25-3p在lps诱导的心肌损伤中的作用机制。方法:采用LPS处理大鼠和H9C2细胞，分别建立体内和体外心肌损伤模型。定量逆转录-聚合酶链反应检测OIP5-AS1和miR-25-3p的表达水平。采用酶联免疫吸附法测定血清IL-6、TNF-α水平。OIP5-AS1与miR-25-3p/NOX4的关系通过荧光素酶报告基因法和/或RNA免疫沉淀法确定。流式细胞术检测细胞凋亡率，3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2- h -溴化四唑试验检测细胞活力。Western blot检测Bax、Bcl-2、caspase3、c-caspase3、NOX4、p-NF-κB p65/NF-κB p65蛋白表达水平。结果:lps诱导的大鼠心肌组织和lps处理的H9C2细胞中，OIP5-AS1上调，miR-25-3p下调。敲低OIP5-AS1可减轻lps诱导大鼠心肌损伤。在体内，OIP5-AS1的敲低也能抑制心肌细胞的炎症和凋亡，这一点随后在体外实验中得到了证实。此外，OIP5-AS1靶向miR-25-3p。MiR-25-3p模拟物逆转了OIP5-AS1过表达促进细胞凋亡和炎症以及抑制细胞活力的作用。此外，在lps诱导的H9C2细胞中，miR-25-3p模拟物阻断了NOX4/NF-κB信号通路。结论:沉默lncRNA OIP5-AS1可通过调节miR-25-3p减轻lps诱导的心肌损伤。

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来源期刊

Analytical Cellular Pathology ONCOLOGY-CELL BIOLOGY

CiteScore

4.90

自引率

3.10%

发文量

审稿时长

16 weeks

期刊介绍： Analytical Cellular Pathology is a peer-reviewed, Open Access journal that provides a forum for scientists, medical practitioners and pathologists working in the area of cellular pathology. The journal publishes original research articles, review articles, and clinical studies related to cytology, carcinogenesis, cell receptors, biomarkers, diagnostic pathology, immunopathology, and hematology.