Tilianin pretreatment prevents myocardial ischemia-reperfusion injury via preservation of mitochondrial function in rat heart.

BACKGROUND

Tilianin has been demonstrated to exert protective effects on the heart against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the mitochondria during myocardial I/R is unclear.

METHODS

In this study, we demonstrated that pretreatment with Tilianin dose-dependently raised the levels of ATP of the myocardium, and protected the microstructures and functions of mitochondria in rats. Furthermore, the cytoprotective effect of Tilianin has been confirmed in vivo and in the H9c2 cardiomyoblast cell line with enhancing activities of the mitochondria, controlling the levels of Ca2+ and reactive oxygen species (ROS), and inhibiting the expression of caspase-3 and AIF in cytoplasm.

CONCLUSIONS

In conclusion, the study suggests that Tilianin may be of clinical value for the protective effects of cardiomyocytes and mitochondria by inhibiting myocardium energy metabolism and apoptosis during myocardial ischemia-reperfusion injury (MIRI).