Cardioprotective Effect of Scleria lithosperma on Doxorubicin-induced Cardiotoxicity in Wistar Albino Rats

Aim: The present study was designed to evaluate the protective effects of ethanolic extract of whole plant of Scleria lithosperma (EEWSL) against doxorubicin-induced cardiotoxicity in rats.

Methodology: EEWSL was orally administrated in two different doses (250 mg/kg/day and 500 mg/kg/day) to wistar albino rats for 28 days and then intoxicated with doxorubicin (20 mg/kg) by intraperitoneal injection to induce myocardial toxicity. Lipid profile (Total cholesterol (TC), Triglyceride (TG), Low Density Lipoprotein-cholesterol (LDL-C) and High Density Lipoprotein-cholesterol (HDL-C)), antioxidant marker enzymes (Cardiac superoxide dismutase, Cardiac catalase activity, Glutathione reductase activity) and liver diagnostic marker enzymes (SALT, SAST, Creatine phosphokinase, Lactate dehydrogenase) were measured at the end of experimental period. Histopathological changes of heart were observed with optical microscopy.

Results: Doxorubicin (DOX) alone injected rats showed altered lipid profile and significant increase in serum markers (Serum glutamate pyruvate transaminase, Serum glutamate oxaloacetate tranaminase, Lactate dehydrogenase and Creatine phosphokinase) of heart injury and lipid peroxidation. Levels of endogenous antioxidant enzymes were also decreased when compared to normal control group. EEWSL pretreatment of DOX-challenged rats significantly reduced the risk of cardiotoxicity by decreasing the levels of liver diagnostic marker enzymes, TC, TG, LDL-C and VLDL-C and increasing the levels of HDL-C and antioxidant enzymes (cardiac superoxide dismutase, Cardiac catalase activity, Glutathione reductase activity) Histopathology of DOX- induced heart of rats pretreated with EEWSL showed a significant recovery from necrosis.

Conclusion: Current findings suggest that EEWSL has protective effects against DOX induced cardiotoxicity and this can be attributed due to its antioxidant properties and inhibition of lipid peroxidation.