The Action and Mechanism of Action of Ligustrazine Promotes on Myocardial Infarction? An Animal Study

Purpose: This study investigated the action and mechanism of Ligustrazine (TMP) on myocardial infarction (MI).Methods: A MI model was established, using adult male Sprague-Dawley (SD) rats. Heart function indicators were measured, using echocardiography. Real-time reverse transcription polymerase chain reaction (qRT-PCR) assay was used, to measure the micro ribonucleic acid-181a-5p (miR-181a-5p) expression. The therapeutic effect of (miR-181a-5p) on MI mice was investigated, using western blot. Hematoxylin-eosin (HE) staining was used, to determine the cross-section area (CSA) of myocardial cells. The expression of inflammatory cytokines was determined, using ELISA (enzyme-linked immunosorbent assay) kits.Results: The left ventricular ejection fraction (LVEF), and left ventricular fractional shortening (LVFS) significantly declined while the left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) obviously increased 14 days after MI was established. TMP treatment significantly promoted cardiac function of MI rats. The CSA was significantly elevated in MI rats and TMP treatment significantly abated CSA expression. TMP treatment significantly inhibited the inflammatory cytokines and significantly up-regulated apoptosis-related protein of cardiac tissues in MI rats. In addition, miR-181a-5p significantly increased in MI rats, significantly reversing the therapeutic effect of TMP on MI rats. Signal transducer and activator of transcription 3 (STAT3) was predicted to combine with miR-181a-5p.Conclusions: TMP treatment significantly promoted cardiac function and inhibited the levels of inflammatory cytokines to alleviate MI, by regulating the miR-181a-5p/STAT3 axis.