Anti-inflammatory effect of protocatechuic aldehyde on myocardial ischemia/reperfusion injury in vivo and in vitro.

Myocardial ischemia/reperfusion (MI/R) injury, in which inflammatory response plays a vital role, is frequently encountered in clinical practice. The present study was aimed to investigate the anti-inflammatory effect and the possible mechanism of protocatechuic aldehyde (PAl) on MI/R injury both in vivo and in vitro. The rat model of MI/R injury was induced by ligation of the left anterior descending coronary artery for 30 min, followed by 3-h reperfusion, and pretreatment with PAl could protect the heart from MI/R injury by reducing myocardial infarct size and the activities of creatine kinase-MB and cardiac troponin I (cTn-I) in serum. Also, PAl administration markedly reduced cellular injury induced by simulated ischemia/reperfusion (SI/R) in cultured neonatal rat cardiomyocytes, which was evidenced by increased cell viability, reduced lactate dehydrogenase and cTn-I activities in the culture medium, and greatly decreased percentage of cell apoptosis. Moreover, the levels of tumor necrosis factor-α, interleukin-6, intracellular adhesion molecule-1, phosphorylated IκB-α, and the nuclear translocation of nuclear factor-kappa B (NF-κB) were all evidently decreased by PAl both in vivo and in vitro. Taken together, these observations suggested that PAl could exert great protective effects against MI/R injury in rats and SI/R injury in cultured neonatal rat cardiomyocytes, and the cardioprotective mechanism might be involved in the suppression of inflammatory response via inhibiting the NF-κB signaling pathway.