Liriodendrin alleviates myocardial ischemia‑reperfusion injury via partially attenuating apoptosis, inflammation and mitochondria damage in rats

Myocardial ischemia‑reperfusion (I/R) injury may lead to dysfunction of signaling pathways related to cell apoptosis, inflammation, oxidative stress, and mitochondrial damage. The present study investigated the defensive effect of liriodendrin, as a natural product isolated from <i>Linaria vulgaris</i>, on reperfusion injury in rats and the underlying mechanisms involved in this process. An <i>in vivo</i> rat model of I/R constructed by ligation of the left anterior descending artery, as well as an <i>in vitro</i> model using H9C2 cells under hypoxic conditions, was established to assess the cardioprotective effects of liriodendrin. The biomarkers of myocardial damage, oxidative stress, and inflammatory response were measured with enzyme‑linked immunosorbent assay (ELISA). Gene and protein expression were detected by reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting. Mitochondrial morphology was observed by electron microscopy. The levels of creatine kinase isoenzymes and cardiac troponin T were significantly elevated in the I/R compared with the sham group; liriodendrin mitigated this elevation. The liriodendrin group exhibited a significant reduction in myocardial tissue apoptosis, as indicated by immunohistochemical staining and western blotting. Additionally, ELISA indicated that the I/R group had higher levels of reactive oxygen species (ROS) compared with the liriodendrin group, while the liriodendrin group had higher levels of superoxide dismutase. The <i>in vitro</i> experiments demonstrated that liriodendrin ameliorated hypoxia‑induced injury to mitochondria and suppressed the activation of nuclear factor-κB and B-cell lymphoma-2 associated X protein (Bax). Therefore, the present study demonstrated that liriodendrin impeded ROS‑associated metabolic disorders, maintained mitochondrial homeostasis and partially alleviated cardiomyocyte apoptosis by inhibiting the Bax signaling pathway.