ABSTRACT

In this study, the effects of Prunus laurocerasus fruit extract (PLE), which is known for its high levels of phenolic compounds and antioxidant efficiency, on doxorubicin (DXR)-induced cardiotoxicity were examined.

Male Sprague-Dawley rats were randomly assigned to the Control, DXR, PLE500+DXR, and PLE1000+DXR groups (n=6). PLE was orally administered to the animals in the PLE500+DXR (500 mg/kg) and PLE1000+DXR (1000 mg/kg) groups for 2 weeks. DXR was injected (15 mg/kg, intraperitoneally) 2 days before sacrification in the DXR, PLE500+DXR, and PLE1000+DXR groups. At the end of the study period, serum troponin I levels, myocardial superoxide dismutase (SOD) and catalase (CAT) activities, malondialdehyde (MDA), glutathione (GSH), glucose-regulated protein (GRP)78, and pro-caspase 12 levels were measured.

In the DXR group, serum troponin I concentration significantly increased (p<0.001), however PLE treatment significantly reduced this DXR-induced increment (p<0.001 and p<0.05 in the PLE500+DXR and PLE1000+DXR groups, respectively). DXR-induced increase in myocardial MDA (p<0.001) significantly reduced in the PLE500+DXR (p<0.001) and PLE1000+DXR (p<0.001) groups. However, DXR-induced changes, such as GSH depletion (p<0.001), reduced CAT (p<0.001) and SOD (p<0.001) activities, increased GRP78 (p<0.01) and decreased pro-caspase 12 (p<0.001) levels, were not significantly affected by PLE treatment.

The present results indicate that pretreatment with PLE reduced, but not completely prevented, cardiac damage induced by DXR. While a reduction in oxidative stress appears to play a role in the partial protective effect of PLE treatment, endoplasmic reticulum stress appears to have no role. Further research is necessary to understand the mechanisms of action underlying PLE treatment.