Cardioprotective effect of (-)-α-Bisabolol in animal model of myocardial infarction

Myocardial infarction characterized by an imbalance of coronary blood supply and demands in myocardial cell death involves oxidative stress and subsequent inflammation. Despite of tremendous development in interventional cardiology and pharmacological agents, novel agents are needed for the prevention and treatment of myocardial infarction. In such efforts, (-)-α-Bisabolol, a sesquiterpene alcohol has received enormous interest being present in the essential oil of a variety of dietary plants, including chamomile. Recently, it showed gastroprotective, antimicrobial, anticancer and anti-inflammatory properties. Thus, the present study was aimed to investigate the cardioprotective activity of Bisabolol in a clinically relevant animal model of myocardial infarction induced by isoproterenol. Being a synthetic catecholamine, isoproterenol at supra-physiological doses induces myocardial injury similar to that of human myocardial infarction. In rats, two subcutaneous injections of isoproterenol (85 mg/kg) at an interval of 24 hour induced myocardial injury and Bisabolol (20 mg/kg) was administered orally for 15 days. The injections of isoproterenol induced depletion of endogenous non enzymatic and enzymatic antioxidants (glutathione, superoxide dismutase, catalase, glutathione cycle enzymes), and serum marker enzymes (creatine phosphokinase-MB, lactate dehydrogenase) from myocardium along with raised lipid peroxidation (malondialdehyde) and enhanced levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). Isoproterenol also produced hemodynamic (arterial pressures and heart rate) impairment and caused histopathological alterations in myocardium. Treatment with (-)-α-Bisabolol prevented the depletion of endogenous antioxidants, augmented enzymatic antioxidants and restored myocardial enzymes, therefore reduced myocyte injury marker enzymes and inhibited lipid peroxidation. Bisabolol treatment also corrected the altered hemodynamics, reduced induction of pro-inflammatory cytokines and salvaged myocardium evidenced by reduced myonecrosis, edema and infiltration of inflammatory cells. The present study demonstrates that Bisabolol exerts cardioprotective effect by mitigating oxidative stress, augmenting endogenous antioxidants and maintaining structural integrity. The results indicate that dietary available Bisabolol may be useful to prevent the onset and progression of myocardial injury.