Leonurine Attenuates Myocardial Fibrosis Through Upregulation of miR-29a-3p in Mice Post-myocardial Infarction.

摘要: ABSTRACT Myocardial fibrosis (MF) is a pathological process that accelerates cardiac remodeling in myocardial infarction (MI), and miR-29 has become one of the foci research into MF. As an alkaloid extracted from Herba leonuri, leonurine (LE) been found to be effective natural active ingredient for inhibiting many preclinical experiments. However, whether LE protects against MF after MI through modifying remains unclear. The present study aimed investigate therapeutic effects on MF, elucidate underlying mechanisms involved. A mouse model was established, followed by administration 4 weeks. We effectively improved function, attenuated mice post-MI. In vitro, simultaneously inhibited proliferation migration neonatal fibroblasts (CFs) exposed angiotensin II (Ang II), activation collagen synthesis myofibroblast generation markedly suppressed LE. Notably, we all mature family members were downregulated tissues post-MI, whereas significantly upregulated miR-29a-3p expression, such upregulation also detected LE-treated CFs under Ang stimulation. Knockdown specific miRNA inhibitor protein levels TGF-β, III, I CFs, completely reversed antifibrotic CFs. Our suggests exerts cardioprotective possibly miR-29a-3p.