Objective: Cardiovascular disease is the major cause of mortality and morbidity. Various studies have shown that oxidative stress plays a major role in myocardial infarction. This study investigated the cardio-protective effect of noscapine against isoprenaline-induced cardiotoxicity.
Materials and methods: Rats received noscapine (5 and 50 mg/kg) or vitamin E (positive control) orally from day 1 to 9. In the pre-treatment group, isoprenaline was injected subcutaneously at a dose of 85 mg/kg on the 8^th and 9^th days. In the co-treatment group, isoprenaline was administered on the 2^nd and 3^rd days. On the 10^th day, rats were anesthetized, and blood was collected from the heart to determine lactate dehydrogenase (LDH), creatine kinase muscle-brain (CK-MB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lipid profile. The levels of superoxide dismutase (SOD), catalase, malondialdehyde (MDA), and thiol were measured in cardiac tissue. A histopathological study was also performed on cardiac tissue.
Results: Isoprenaline increased LDH, CK-MB, and MDA, while reducing SOD, thiol, and catalase (P<0.001 for all cases). Isoprenaline led to the infiltration of inflammatory cells and necrosis. In pre- and co-treatment groups, noscapine reduced MDA, lipid profile, and cardiac markers while increasing anti-oxidant activity and high density lipoprotein (HDL). Vitamin E, as a positive control, decreased lipid peroxidation and oxidative stress, and modulated lipid profile. 
Conclusion: Noscapine attenuated isoprenaline-induced cardiac toxicity in the tissue. The protective effect of noscapine was partly mediated by reducing oxidative stress, suggesting a role in the modulation of isoprenaline-induced cardiotoxicity.