β-Caryophyllene inhibits Fas- receptor and caspase-mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction.

We planned to appraise the effects of β-caryophyllene on Fas- receptor and caspase-mediated apoptosis signaling pathway and endothelial dysfunction in rats infarcted with isoproterenol. Rats were induced myocardial infarction by using isoproterenol (100 mg/kg body weight [b.w]). Serum creatine kinase-MB, serum cardiac troponin-T, heart weight, heart rate, and heart lipid peroxidation were greatly (p < 0.05) augmented, while heart enzymatic antioxidants and plasma nonenzymatic antioxidants were greatly (p < 0.05) lessened in isoproterenol-treated rats. Reverse transcription-polymerase chain reaction study revealed augmented expressions of Fas-receptor and caspases 8, 9, and 3 genes in myocardial infarcted rats. Furthermore, iNOS protein expression was amplified and eNOS protein was lessened in the myocardial infarcted heart. Three weeks pre- and cotreatment with β-caryophyllene (20 mg/kg b.w) greatly (p < 0.05) protected isoproterenol-treated rats against these altered structural, biochemical, molecular, and immunohistochemical parameters, by its anti-cardiac hypertrophic, anti-tachycardial, antioxidant, anti-apoptotic, and anti-endothelial dysfunction effects. In conclusion, these findings projected the use of β-caryophyllene for the therapy of human myocardial infarction after clinical trials.