Fucoxanthin averts isoprenaline hydrochloride-induced myocardial infarction in rats

Abstract

Background: In this current investigation, we aimed to assess the efficacy of natural antioxidant fucoxanthin against the myocardial infarction since it can be consumed as a regular diet. Objective: In this scientific investigation, we planned to investigate the curative effectual of fucoxanthin on isoprenaline hydrochloride provoked myocardial infarction on the experimental rats. Materials and Methods: Healthy Wistar albino rats were grouped into control, fucoxanthin alone, myocardial infarction induced, and myocardial infarction induced pretreated with fucoxanthin. The control rats were treated with a standard food diet, whereas fucoxanthin alone group rats were treated with 50 mg/kg/bwt of fucoxanthin along with standard diet. Myocardial infarction-induced groups were treated with 85 mg/kg/bwt of isoprenaline hydrochloride to induce myocardial infarction on the 29th and 30th days of the treatment period. Group IV rats were pretreated with 50 mg/kg/bwt of fucoxanthin from day 1 of experiment and on the 29th and 30th days of treatment period treated with 85 mg/kg/bwt of isoprenaline hydrochloride to induce myocardial infarction. Results: The fucoxanthin possessed effective cardioprotective activity in mycardiac infarction-induced rats. Fucoxanthin treatment reduced the statuses of cardiac troponin T and cardiac troponin I on myocardial infarction provoked rats; also, it exhibited the reduced Thiobarbituric acid reactive substances (TBARS) level in the rats. The antioxidant status such as superoxide dismutase, catalase, and glutathione peroxidase was extensively elevated in the myocardial infarction-induced fucoxanthin pretreated rats. Myocardial infarction-induced fucoxanthin pretreated rats shows decreased statuses of Na+/K+ ATPase and increase on the Na+/K+ ATPase level. Conclusion: Our results confirmed that fucoxanthin is a potent cardioprotective drug which increases the antioxidant levels and decreases the oxidative stress and inflammation during myocardial infarction.