Abstract: Objective To explore the potential role and mechanism of miR-30a in myocardial fibrosis after myocardial infarction(MI)．Methods We constructed the AAV plasmid vector which carried the miR-30a gene of rat .The recombinant plasmid was detected by gene sequencing, enzyme digestion and PCR. Virus was packaged in HEK293 cells and virus titer was determined after extraction and purification by PCR. PBS fluid , rAAV9-miR-30a-NC and rAAV9-miR-30a were transmited to the rat hearts of PBS group，miR-30a-NC group and miR-30a group respectively through transcoronary infusion before anterior descending coronary artery ligation．Sham group was set up at the same time. After 4 weeks, heart function was monitored by serial echocardiography, including fractional shortening (FS), and left ventricular ejection fraction (LVEF). Masson staining was used to calculate collagen volume fraction (CVF). The expression of collagen I and III were detected by immunohistochemistry. The mRNA level of miR-30a, TGF-?1 and CTGF were detected by real-time PCR analysis. The protein level of TGF-?1 and CTGF were detected by western blot analysis. ResultsThe cardiac function of miR-30a group was improved significantly compared with PBS group and miR-30a-NC group (P<0.05). The levels of CVF，collagen I,III expression and Collagen I/III ratio in miR-30a group were significantly lower than PBS group and miR-30a-NC group(P<0.01). The mRNA and protein level of TGF-?1 and CTGF in miR-30a group were reduced significantly than PBS group and miR-30a-NC group (P<0.001). ConclusionsThe overexpression of miR-30a after MI could reduce the mRNA and protein level of TGF-?1 and CTGF, so as to suppress myocardial fibrosis and improve cardiac function．

Key words: miR-30a, myocardial infarction, myocardial fibrosis, transforming growth factor-β1, connective tissue growth factor