β-caryophyllene blocks reactive oxygen species-mediated hyperlipidemia in isoproterenol-induced myocardial infarcted rats.

Myocardial infarction (MI) is a leading cause of death. Lipid-lowering interventions have been shown to decrease coronary events and mortality of MI and heart failure. In this investigation, we assessed the anti-hyperlipidemic effects of β-caryophyllene in isoproterenol-induced myocardial infarcted rats. β-Caryophyllene (20 mg/kg body weight) pre-and co-treatment was given to rats orally, daily, for 3 weeks. Isoproterenol (100 mg/kg body weight) was administered to rats to induce MI. The levels of serum cardiac troponins T and I, serum and heart total cholesterol, triglycerides, free fatty acids, and the levels of serum low-density and very low-density lipoprotein-cholesterols were augmented, and the level of serum high-density lipoprotein-cholesterol was lessened in myocardial infarcted rats. Further, the activity/levels of liver 3-hydroxy-3-methylglutaryl-coenzyme A reductase and plasma thiobarbituric acid reactive substances were amplified and the activity/levels of heart glutathione -S- transferase, vitamin C, and vitamin E were lessened by isoproterenol. A down-regulated expression of liver sterol regulatory element-binding protein-2 and liver low-density lipoprotein-receptor genes was observed by a reverse transcription-polymerase chain reaction study. Moreover, histopathology of Sudan III staining revealed an accumulation of fats in the heart of isoproterenol-induced rats. Nevertheless, β-caryophyllene pre-and co-treatment blocked alterations in all the parameters examined in isoproterenol-induced rats and inhibited the risk of MI. Moreover, the in vitro study revealed the potent free radical scavenging and antioxidant effects of β-caryophyllene. β-Caryophyllene's antioxidant and anti-hyperlipidemic properties are the possible mechanisms for the observed protective effects in this investigation.