Department of Traditional Chinese Medicine, Yantaishan Hospital, Yantai, China.
Department of Medical Security Center, PLA Rocket Force Characteristic Medical Center, Beijing, China.
Dis Markers. 2021 Nov 29;2021:8740831. doi: 10.1155/2021/8740831. eCollection 2021.
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).
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.
Through upregulating miR-205-3p and downregulating TGF-1, TSN alleviates cardiac fibrosis and improves ventricular remodeling following MI.
阐述丹参酮 IIA（TSN）在心肌梗死后调节心脏结构和功能中的作用，以及 miR-205-3p 在 TSN 诱导的抗纤维化作用对心室重构的影响。
选择 100 例心肌梗死患者，随机分为两组，分别给予 TSN（TSN 组，n=50）或常规治疗（对照组，n=50）。检测每位患者的血浆 miR-205-3p 和 TGF-1 水平。分别在心肌梗死后 1 天、2 周和 4 周对每位患者进行超声心动图检查，记录左室舒张末期内径（LVIDd）、左室收缩末期内径（LVIDs）和左室射血分数（LVEF）。采用 RNA 结合蛋白免疫沉淀（RIP）试验检测 miR-205-3p 和 TGF-1 之间的相互作用。在诱导 TGF-1 和/或 10μM TSN 后，用实时定量聚合酶链反应（qRT-PCR）检测心肌成纤维细胞中 miR-205-3p、Col1a1 和 Col3a1 的相对水平。
与对照组相比，TSN 组 MI 患者血浆中 miR-205-3p 和 TGF-1 下调。与心肌梗死后 1 天相比，TSN 组患者在 2 周和 4 周时 LVIDd 和 LVIDs 降低，EF 升高。miR-205-3p 可与 TGF-1 负性相互作用。TSN 诱导可消除 TGF-1 下调 miR-205-3p 以及上调心肌成纤维细胞中 Col1a1 和 Col3a1 的调节作用。
通过上调 miR-205-3p 和下调 TGF-1，TSN 可减轻心肌梗死后的心肌纤维化，改善心室重构。
