Capparis spinosa reduces cyclophosphamide-induced cardiotoxicity via modulation of oxidative stress

Object Cyclophosphamide is an anti-neoplastic drug that, at high doses, can lead to cardiotoxicity in patients. The most important mechanism of toxicity is the reactive oxygen species production. However, anti-oxidant agents can have beneficial effects in reducing toxicity. Recent investigations have reported the anti-oxidant activities of Capparis spinosa , which originates from west or central Asia. In this study, we assayed its effects against cyclophosphamide-induced cardiotoxicity. Method The various groups are including control, cyclophosphamide, and therapeutic. In treatment groups, the extract (100 and 300 mg/kg) was given via gavage for 21 days. Cyclophosphamide was injected intraperitoneally on the 8th day as a single dose. On 22nd day, blood samples were recived from the heart to separate serum for measurement of lactate dehydrogenase (LDH) and creatinine kinase (CPK). The cardiac tissue was isolated to study biochemical and histopathological changes. Results Cyclophosphamide elevated the level of LDH and CPK as significantly (p < 0.001), production of malondialdehyde (MDA) (p < 0.001) while attenuted superoxide dismutase (SOD) (p < 0.001) and content of thiol (p < 0.001). Capparis spinose prevented cyclophosphamide toxicity via attenuation of LDH, CPK, and MDA at two doses (p < 0.001) while increasing thiol amount and SOD activity at the concentration of 300 mg/kg (p < 0.01). Also, histopathological studies showed Capparis spinosa reduced cardiac damage following cyclophosphamide. Conclusion Capparis spinosa can reduce cyclophosphamide-induced cardiotoxicity via the decreasing of oxidative stress and peroxidation of lipids because it contains phenolic compounds that can scavenge free radicals and attenuate cardiac damage.