Tanshinone IIA improves ventricular remodeling following cardiac infarction by regulating miR-205-3p.

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PMID: Dis Markers. 2021 ;2021:8740831. Epub 2021 Nov 29. PMID: 34880957 Abstract Title: Tanshinone IIA Improves Ventricular Remodeling following Cardiac Infarction by Regulating miR-205-3p. Abstract: 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.. One hundred MI patients were randomly assigned into two groups, and they were treated with TSN (TSN group,= 50) or conventional therapy (control group,= 50). Plasma levels of miR-205-3p and TGF-1 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-1 was examined by the RNA-Binding Protein Immunoprecipitation (RIP) assay. After induction of TGF-1 and/or 10 L 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-1 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-1. TSN induction abolished the regulatory effects of TGF-1 on downregulating miR-205-3p and upregulating Col1a1 and Col3a1 in cardiac fibroblasts.Conclusions: Through upregulating miR-205-3p and downregulating TGF-1, TSN alleviates cardiac fibrosis and improves ventricular remodeling following MI.
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