Micheliolide alleviates oxygen-glucose deprivation/reoxygenation-evoked inflammation and ROS production in H9c2 cells.

Myocardial ischemia/reperfusion (I/R) injury can lead to substantial cardiac damage and pose a significant threat to human health and survival. Micheliolide (MCL), a sesquiterpene lactone extracted from Michelia (Magnoliaceae), has been reported to exhibit anti-inflammatory, anti-fibrotic and anti-oxidant properties. However, the potential regulatory role of MCL in the progression of myocardial I/R injury remains unclear. In this study, we demonstrated that MCL improved cell viability in H9c2 cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Furthermore, MCL treatment significantly attenuated the inflammatory response induced by OGD/R in H9c2 cells. OGD/R stimulation markedly increased reactive oxygen species (ROS) production, which was effectively reduced by MCL administration. In addition, MCL inhibited the elevated apoptosis observed in OGD/R-treated H9c2 cells. Mechanistically, MCL suppressed the activation of the NF-κB signaling pathway following OGD/R exposure. In summary, this study provides the first evidence that MCL mitigates OGD/R-induced inflammation and oxidative stress in H9c2 cells, suggesting its potential as a therapeutic candidate for the treatment of myocardial I/R injury.