Abstract: [Abstract] Objective  To investigate the protective effect of miRNA-21 in myocardial ischemic postconditioning, and to explore the interaction effects in the mechanism of myocardial protection with JAK2-STAT3 pathway in ischemic postconditioning. Methods   The healthy adult male Wistar rats (body weight 240~280g) were randomly divided into five groups:Sham group, schemia-reperfusion injury group (I/R group), Ischemic postconditioning group (PostC group), schemic postconditioning + antagomiR-21 treatment group (PostC + antagomiR-21 group), and Ischemic postconditioning + AG490 group (PostC + AG490 group). In situ terminal deoxynucleotidyl transferase labeling (TUNEL) staining was used to analysis myocardial apoptosis index; Western-blot was used to detect total STAT3 (t-stat3) and phospho-STAT3 (p-stat3) protein levels.miRNA-21 levels were detected by quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR). Results   Compared with the I / R group after reperfusion,ischemic postconditioning significantly reduced the apoptosis index, dramatically increased the expression levels of miRNA-21 and markedly up-regulated the stat3 phosphorylation levels. AntagomiR-21 significantly weaken the protective effect of ischemic postconditioning. PostC + antagomiR-21 group compared with PostC, STAT3 phosphorylation levels were observably lower. Compared with postC group, STAT3 phosphorylation levels and miRNA-21 were significantly lower in PostC+AG490 group. Conclusion   miRNA-21 play a regulatory role in myocardial ischemic postconditioning. STAT3 and miRNA-21 in post-processing adaptive mechanism there may be some kind of loop regulatory mechanism. But the reciprocal of the detailed regulation mechanism is unclear, pending further study.

Key words: myocardial reperfusion injury, microRNAs, in situ nick-end labeling, cell cycles, STAT3 transcription factor, rats, Wistar, 缺血后处理