ArticleArchives of medical science : AMS2026
Protective effect of casticin in myocardial ischemia/reperfusion injury in rats via attenuation of oxidative stress and inflammation.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: 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 κ-light-chain-enhancer of activated B cells (NF-κB). Results: 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/dt Conclusions: 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-κB and iNOS in western blot analysis.
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