Protective effect of quercetin on secondary cardiomyocyte injury induced by mechanical trauma

AIM To observe the effect of quercetin on secondary cardiomyocyte apoptosis and cardiac dysfunction induced by mechanical trauma in rats and discuss its mechanism. METHODSThe experiment was conducted in vivo and in vitro. First, 120 adult male Sprague Dawley rats were randomly divided into four groups: sham group, trauma group, trauma+qucercetin group and trauma+vehicle group for experiments in vivo. We used Noble-Collip drum to prepare the mechanical trauma model of rats. We then recorded the changes of the left ventricular diastolic pressure with the intubation from the right common carotid artery to the left ventricle to identify the protective effect of quercetin on rat cardiac function. MTT assay was used to evaluate the effects of quercetin on the survival rate of H9c2 cells induced by trauma plasma. Using TUNEL staining, we assessed the apoptosis degree of cardiomyocytes. Reactive oxygen species (ROS) produced by H9c2 cells before and after the administration of quercetin was detected by microplate reader to substantiate the protective effects of quercetin. We used laser scanning confocal microscope to observe the cardiomyocytes marked by Fluo-4AM to determine the changes of intracellular Ca2+. RESULTSLVDP, +dP/dtmax and -dP/dtmax in trauma group and trauma+vehicle group significantly decreased, and those in trauma+quercetin group increased compared with those in sham group (P<0.01). Under tested concentrations, quercetin had no toxicity to H9c2 cells and could obviously inhibit the damage of trauma plasma. The apoptosis index of cardiomyocytes in the trauma+quercetin group was lower than that in the trauma group (P<0.01). By detecting the oxide in H9c2 cells, we observed that quercetin reduced MT-induced overproduction of ROS. The concentration of intracellular calcium increased when cultured with trauma plasma and after given a certain concentration of quercetin, the concentration of intracellular calcium decreased. CONCLUSIONUsed at an appropriate concentration, quercetin can reduce the overproduction of ROS induced by MT and inhibit MT-initiated Ca2+ influx. Quercetin can also inhibit myocardial apoptosis, improve heart function after MT and exert some protective effect on the heart.