Myocardial ischemic/reperfusion injury is the main prognostic factor after myocardial infarction. However, by the time reperfusion is achieved, the cardiac tissues have already undergone necrosis and initiated inflammation and oxidative stress. Therefore, the present study aimed to evaluate the beneficial effect of casticin (CST) on myocardial ischemia/ reperfusion (MI/R) injury and to explore its mechanism of action.

Material and methods:
MI/R injury was induced using 30-min left anterior descending coronary artery (LAD) occlusion followed by 4 h reperfusion. CST was administered to rats before reperfusion. The outcome of CST was determined according to various indices of oxidative stress, inflammation, apoptotic genes and nuclear factor k-light-chain-enhancer of activated B cells (NF-kB).

The results suggested that CST causes significant improvement in left ventricular systolic pressure (LVSP) and derivative of pressure over time of maximal rate of rise of (usually) left ventricular pressure (± dp/dtmax) with reduction of left ventricular end-diastolic pressure (LVEDP). It also reduces increased ST segment together with restoration of the changes in RR interval and QRS complex. The histopathological analysis of cardiac tissue further corroborated the effect of CST. It also causes improvement of the antioxidant system by reducing malondialdehyde (MDA) level with increase in superoxide dismutase (SOD) and glutathione peroxidase (GPx). The levels of cytokines (TNF-α, IL-1β and IL-6) were also found to be reduced upon CST treatment. The expression of NF-kB, inducible nitric oxide synthase (iNOS) and BCL2-associated X protein (Bax) was found to be reduced in the CST treated group together with an increase in Bcl-2.

Collectively, the results of the study demonstrated that casticin protects rats from MI/R damage possibly via attenuation of oxidative stress, the inflammatory response and apoptosis. It was also shown to inhibit NF-kB and iNOS in western blot analysis.