Tanshinone IIA Improves Ventricular Remodeling following Cardiac Infarction by Regulating miR-205-3p

• Published in: Disease markers 2021, Vol.2021, p.8740831-6
• Main Authors: Qiao, Peng, Xu, Jie, Liu, Xueni, Li, Xuehan
• Format: Article
• Language: English
• Subjects: Abietanes - pharmacology; Animals; Cancer; Cardiomyocytes; Cardiovascular disease; Cell culture; Cells, Cultured; Collagen (type I); Echocardiography; Electrocardiography; Female; Fibroblasts; Fibrosis; Gene Expression Regulation; Heart; Heart attacks; Humans; Hypertension; Immunoprecipitation; Male; MicroRNAs - genetics; Middle Aged; Mortality; Myocardial infarction; Myocardial Infarction - metabolism; Myocardial Infarction - physiopathology; Plasma levels; Polymerase chain reaction; Rats; RNA-binding protein; Structure-function relationships; Tanshinones; Transforming Growth Factor beta1 - metabolism; Transforming growth factor-b1; Tumors; Ultrasonic imaging; Ventricle; Ventricular Function, Left - drug effects; Ventricular Remodeling - drug effects
• ISSN: 0278-0240; 1875-8630
• DOI: 10.1155/2021/8740831

Objective. To illustrate the role of tanshinone IIA (TSN) in regulating cardiac structure and function following myocardial infarction (MI) and the involvement of miR-205-3p in TSN-induced antifibrosis effect on ventricular remodeling. Patients and Methods. One hundred MI patients were randomly assigned into two groups, and they were treated with TSN (TSN group, n=50) or conventional therapy (control group, n=50). Plasma levels of miR-205-3p and TGF-β1 were detected in each patient. Echocardiography was conducted in each patient at post-MI 1 day, 2 weeks, and 4 weeks, respectively, for recording LVIDd (left ventricular internal-diastolic diameter), LVIDs (left ventricular internal-systolic diameter), and LVEF (left ventricular ejection fraction). The interaction between miR-205-3p and TGF-β1 was examined by the RNA-Binding Protein Immunoprecipitation (RIP) assay. After induction of TGF-β1 and/or 10 μL of TSN in cardiac fibroblasts, relative levels of miR-205-3p, Col1a1, and Col3a1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Results. Compared with the control group, miR-205-3p and TGF-β1 were downregulated in plasma of MI patients in the TSN group. In the TSN group, LVIDd and LVIDs were reduced, and EF was enhanced at 2 weeks and 4 weeks compared with that at post-MI 1 day. miR-205-3p could negatively interact with TGF-β1. TSN induction abolished the regulatory effects of TGF-β1 on downregulating miR-205-3p and upregulating Col1a1 and Col3a1 in cardiac fibroblasts. Conclusions. Through upregulating miR-205-3p and downregulating TGF-β1, TSN alleviates cardiac fibrosis and improves ventricular remodeling following MI.