BACKGROUND: Sodium ferulate preconditioning can protect myocardial cells, which has been proved in the experiments of isolated rat heart and neonatal rat myocardial cells, but there are few experimental studies regarding adult rat myocardial cells.
OBJECTIVE: To explore the protective effect of sodium ferulate preconditioning on myocardial cells following anoxia-reoxygenation (A/R) in adult rats as well as its mechanism underlying adenosine triphosphate-sensitive potassium (K+ATP) channel .
METHODS: Rat heart was perfused with Langendorff system. The purified adult rat myocardial cells were isolated by collagenase digestion method and then treated with simulated A/R solution, sodium ferulate (SF) as well as glibenclamide (Glib), a K+ATP channel blocker. Then, the myocardial cells were randomly divided into six groups: control group, A/R group, anoxia preconditioning (APC)+A/R group, SF+A/R group, Glib+APC+A/R group and Glib+SF+A/R group.
RESULTS AND CONCLUSION: ①Myocardial cell viability: compared with the control group, the cell viability in the A/R group was significantly decreased (P < 0.01). Compared with the A/R group, the cell viability was significantly increased in the APC+A/R group and SF+A/R group (P < 0.01). The cell viability in the Glib+APC+A/R and Glib+SF+A/R groups had no difference from that of the A/R group, but significantly higher than that of the APC+A/R group (P < 0.01). ②Lactate dehydrogenase activity: the comparison results of lactate dehydrogenase activity were consistent with those of myocardial cell viability among these groups. ③Ultrastructure observation under a transmission electron microscope: the myocardial cells subjected to A/R injury were characterized by mitochondrial swelling, disappearance or deformation of mitochondrial cristae, disruption of nuclear membrane, and nuclear condensation. While the ultrastructure of the myocardial cells in the APC+A/R group and SF+A/R group were changed slightly, exhibiting regular mitochondria with uniform size, intact mitochondrial cristae, intima and extima as well as complete nuclear membrane. The injury was obviously reduced in the APC+A/R group and SF+A/R group compared with the A/R group. The cellular structures in the Glib+APC+A/R group and Glib+SF+A/R group were similar to those in the A/R group. These findings showed that SF preconditioning is effective in protecting the myocardial cells of adult rats from A/R injury and the cardioprotective effect of SF preconditioning is related to the activation of intracellular K+ATP channel.