Notoginsenoside R1 relieves the myocardial infarction via activating the JAK2/STAT3 signaling pathway in vivo and in vitro

ABSTRACT

Myocardial infarction (MI), caused by continuous ischemia and hypoxia of the coronary artery, is one of the major causes of human mortality. This study aimed to investigate the role of notoginsenoside R1 (NGR1) in MI therapy. In vitro and in vivo models of MI were established by hypoxia/reoxygenation (H/R)-treatment of H9C2 cells and through the ligation of the left anterior descending coronary artery of rats, respectively. CCK-8 and EdU assays were performed to measure cell viability and proliferation, respectively. Flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to determine the apoptotic rate of cells. Western blot was used to determine protein expression. The MI area was analyzed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. NGR1 promoted viability and proliferation, and inhibited the apoptotic rate of H/R-treated H9C2 cells. In addition, NGR1 downregulated the protein expression of caspase-3 and Bax, and upregulated Bcl-2 expression in H/R-treated H9C2 cells. The JAK2/STAT3 signaling pathway was activated following NGR1 treatment in vivo and in vitro, and inhibition of the JAK2/STAT3 signaling pathway reversed the effects of NGR1 on H/R-treated H9C2 cells. Finally, NGR1 reduced the area of MI. NGR1 relieved MI in vivo and in vitro by activating the JAK2/STAT3 signaling pathway.

Graphical abstract