Suppr超能文献

心血管疾病患者氧化应激、细胞凋亡及微小RNA - 208a和微小RNA - 1表达的评估

Evaluation of Oxidative Stress, Apoptosis, and Expression of MicroRNA-208a and MicroRNA-1 in Cardiovascular Patients.

作者信息

Mohammadi Asma, Balizadeh Karami Ali Reza, Dehghan Mashtani Vahid, Sahraei Tooba, Bandani Tarashoki Zeinab, Khattavian Ehsan, Mobarak Sara, Moradi Kazerouni Hossein, Radmanesh Esmat

机构信息

Abadan Faculty of Medical Sciences, Abadan, Iran.

Student Research Committee, Abadan Faculty of Medical Sciences, Abadan, Iran.

出版信息

Rep Biochem Mol Biol. 2021 Jul;10(2):183-196. doi: 10.52547/rbmb.10.2.183.

Abstract

BACKGROUND

MicroRNA expression signature and reactive oxygen species (ROS) production have been associated with the development of cardiovascular diseases (CVDs). This study aimed to evaluate oxidative stress, inflammation, apoptosis, and the expression of miRNA-208a and miRNA-1 in cardiovascular patients.

METHODS

The study population included four types of patients (acute coronary syndromes (ACS), myocardial infarction (MI), arrhythmia, and heart failure (HF)), with 10 people in each group, as well as a control group. Quantitative real-time PCR was performed to measure mir-208 and miR-1 expression, the mRNAs of inflammatory mediators (TNFα, iNOS/eNOS), and apoptotic factors (Bax and Bcl2). XOX, MDA, and antioxidant enzymes (CAT, SOD, and GPx) were measured by ZellBio GmbH kits by an ELISA Reader.

RESULTS

The results showed significant decreases in the activity of antioxidant enzymes (CAT, SOD, and Gpx) and a significant increase in the activity of the MDA and XOX in cardiovascular patients. Significant increases in IL-10, iNos, iNOS / eNOS, and TNF-α in cardiovascular patients were also observed. Also, a significant increase in the expression of miR-208 (HF> arrhythmia> ACS> MI) and a significant decrease in the expression of miR-1 (ACS> arrhythmia> HF> MI) were found in all four groups in cardiovascular patients.

CONCLUSION

The results showed increases in oxidative stress, inflammation, apoptotic factors, and in the expression of miR-208a in a variety of cardiovascular patients (ACS, MI, arrhythmia, and HF). It is suggested that future studies determine the relationships that miR-1, miR-208, and oxidative stress indices have with inflammation and apoptosis.

摘要

背景

微小RNA表达特征和活性氧(ROS)产生与心血管疾病(CVD)的发展有关。本研究旨在评估心血管疾病患者的氧化应激、炎症、细胞凋亡以及miRNA - 208a和miRNA - 1的表达。

方法

研究人群包括四类患者(急性冠状动脉综合征(ACS)、心肌梗死(MI)、心律失常和心力衰竭(HF)),每组10人,以及一个对照组。采用定量实时PCR检测mir - 208和miR - 1的表达、炎症介质(TNFα、iNOS/eNOS)和凋亡因子(Bax和Bcl2)的mRNA。使用ZellBio GmbH试剂盒通过酶标仪测量XOX、MDA和抗氧化酶(CAT、SOD和GPx)。

结果

结果显示,心血管疾病患者的抗氧化酶(CAT、SOD和Gpx)活性显著降低,MDA和XOX活性显著升高。还观察到心血管疾病患者的IL - 10、iNos、iNOS / eNOS和TNF -α显著增加。此外,在所有四组心血管疾病患者中均发现miR - 208表达显著增加(HF > 心律失常 > ACS > MI),miR - 1表达显著降低(ACS > 心律失常 > HF > MI)。

结论

结果表明,在多种心血管疾病患者(ACS、MI、心律失常和HF)中,氧化应激、炎症、凋亡因子以及miR - 208a表达均增加。建议未来的研究确定miR - 1、miR - 208和氧化应激指标与炎症和细胞凋亡之间的关系。

相似文献

4
MicroRNA-208a Potentiates Angiotensin II-triggered Cardiac Myoblasts Apoptosis via Inhibiting Nemo-like Kinase (NLK).
Curr Pharm Des. 2016;22(31):4868-4875. doi: 10.2174/1381612822666160210143047.
5
Inhibition of microRNA-184 reduces H2O2-mediated cardiomyocyte injury via targeting FBXO28.
Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):11251-11258. doi: 10.26355/eurrev_202011_23614.
6
MiR-208a aggravates HO-induced cardiomyocyte injury by targeting APC.
Eur J Pharmacol. 2019 Dec 1;864:172668. doi: 10.1016/j.ejphar.2019.172668. Epub 2019 Sep 20.
7
Serum microRNA-499 and microRNA-208a as biomarkers of acute myocardial infarction.
Int J Clin Exp Med. 2014 Jan 15;7(1):136-41. eCollection 2014.
8
Inhibition of microRNA-346 inhibits myocardial inflammation and apoptosis after myocardial infarction via targeting NFIB.
Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11752-11760. doi: 10.26355/eurrev_202011_23827.
10
MicroRNA-323-3p inhibits oxidative stress and apoptosis after myocardial infarction by targeting TGF-β2/JNK pathway.
Eur Rev Med Pharmacol Sci. 2020 Jun;24(12):6961-6970. doi: 10.26355/eurrev_202006_21688.

引用本文的文献

1
Is Inducible Nitric Oxide Synthase (iNOS) Promising as a New Target Against Pulmonary Hypertension?
Antioxidants (Basel). 2025 Mar 21;14(4):377. doi: 10.3390/antiox14040377.
3
Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.
Front Med (Lausanne). 2024 Nov 5;11:1478153. doi: 10.3389/fmed.2024.1478153. eCollection 2024.
5
Cardiovascular Disease and miRNAs: Possible Oxidative Stress-Regulating Roles of miRNAs.
Antioxidants (Basel). 2024 May 27;13(6):656. doi: 10.3390/antiox13060656.
8
Prognostic Value of PtfV1 in Long-Term Outcomes of Patients with Unstable Angina.
Int J Gen Med. 2023 Dec 22;16:6065-6072. doi: 10.2147/IJGM.S439105. eCollection 2023.
10
Functional polymorphism in miR-208 is associated with increased risk for ischemic stroke.
BMC Med Genomics. 2023 Jul 31;16(1):176. doi: 10.1186/s12920-023-01610-y.

本文引用的文献

2
Long Non-Coding HULC and miRNA-372 as Diagnostic Biomarkers in Hepatocellular Carcinoma.
Rep Biochem Mol Biol. 2020 Jul;9(2):230-240. doi: 10.29252/rbmb.9.2.230.
3
Oxidative Stress-Responsive MicroRNAs in Heart Injury.
Int J Mol Sci. 2020 Jan 5;21(1):358. doi: 10.3390/ijms21010358.
4
The Global Burden of Cardiovascular Diseases and Risk Factors: 2020 and Beyond.
J Am Coll Cardiol. 2019 Nov 19;74(20):2529-2532. doi: 10.1016/j.jacc.2019.10.009.
5
Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target?
Nutrients. 2019 Sep 4;11(9):2090. doi: 10.3390/nu11092090.
6
Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease.
Oxid Med Cell Longev. 2019 Jun 23;2019:7092151. doi: 10.1155/2019/7092151. eCollection 2019.
7
Long noncoding RNA/circular noncoding RNA-miRNA-mRNA axes in cardiovascular diseases.
Life Sci. 2019 Sep 15;233:116440. doi: 10.1016/j.lfs.2019.04.066. Epub 2019 Apr 30.
8
Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association.
Circulation. 2019 Mar 5;139(10):e56-e528. doi: 10.1161/CIR.0000000000000659.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验