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Myocardial ischemic/reperfusion injury is the main prognostic factor after myocardial infarction. However, by the time reperfusion isachieved, the cardiac tissues have already undergone necrosis and initiated inflammation and oxidative stress. Therefore, the present study aimedto 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 wasdetermined according to various indices of oxidative stress, inflammation,apoptotic genes and nuclear factor k-light-chain-enhancer of activatedB cells (NF-kB).    Results  The results suggested that CST causes significant improvement inleft ventricular systolic pressure (LVSP) and derivative of pressure over timeof maximal rate of rise of (usually) left ventricular pressure (± dp/dtmax) withreduction of left ventricular end-diastolic pressure (LVEDP). It also reducesincreased ST segment together with restoration of the changes in RR interval and QRS complex. The histopathological analysis of cardiac tissuefurther corroborated the effect of CST. It also causes improvement of theantioxidant system by reducing malondialdehyde (MDA) level with increasein superoxide dismutase (SOD) and glutathione peroxidase (GPx). The levelsof cytokines (TNF-α, IL-1β and IL-6) were also found to be reduced upon CSTtreatment. The expression of NF-kB, inducible nitric oxide synthase (iNOS)and BCL2-associated X protein (Bax) was found to be reduced in the CSTtreated group together with an increase in Bcl-2.    Conclusions  Collectively, the results of the study demonstrated that casticin protects rats from MI/R damage possibly via attenuation of oxidativestress, the inflammatory response and apoptosis. It was also shown to inhibit NF-kB and iNOS in western blot analysis.

Protective effect of casticin in myocardial ischemia/reperfusion injury in rats via attenuation of oxidative stress and inflammation