History

High-anticancer anthracyclines, including doxorubicin, have a long history of usage as chemotherapy drugs. However, its potent cardiotoxic side effects include dilated cardiomyopathy and congestive cardiac failure, which are dose-dependent, restrict its therapeutic usefulness. Due to the presence of various active ingredients like quercetin, marmesinin, kempefrol, and other substances that inhibit cytochrome p450 like xanthotoxin bergapten, imperatorin, and isoimpinellin, Ammi   majus exhibits an antioxidant effect in diabetic nephropathy, myocardial injury. As a result, the objective of this study was to determine whether the seed extract of Ammi1 majus provided cardio-protection against DOX-induced heart injury in mice. 48 mature male mice were separated into six groups and distributed as follows: For 14 days, Group I—the "negative control"—mice received D.W. 2. Group II mice received a single oral dose of 64 mg/kg of Ammi1 majus seeds extract. 3.Group III mice received a single oral daily dose of 128 mg/kg of Ammi1 majus seeds extract. 4.Mice in the positive control (Group IV) group received a single oral dose of 2 ml/kg D.W. every day for 14 days. On day 15, the mice got a single IP dose of 15 mg/kg DOX. The mice were then terminated using anesthetic ether 24 hours later. 5. Group V were given a single dose of 15 mg/kg DOX on day 15 after receiving (64 mg/kg/day) of Ammi1 majus ethanolic extract for 14 days. 6. Finally, group (Group VI) mice received (128 mg/kg of Ammi1 majus seed extract for 14 days, and on day 15 they got a single dosage of 15 mg/kg DOX. The mice were then slaughtered 24 hours after receiving the DOX. To analyze GSH, SOD, GPx, and catalase as indicators of cardiotoxicity, the hearts of mice were collected for the manufacture of tissue homogenate. Analysis of the data showed that mice pre-treated with different doses of Ammi1 majus extract (64 mg and 128 mg/kg/day for 14 days) significantly reduced oxidative stress as compared to group IV of animals intoxicated by DOX as demonstrated by a decrease in (GSH, SOD, GPx, and catalase) levels in heart tissue homogenate.