Protective effect of luteolin on cardiac ischemia/reperfusion injury in rats with myocardial infarction through ERK/JNK signaling pathway

Due to the increased incidence of cardiovascular diseases, the incidence of cardiac ischemia/reperfusion injury (IRI) is also on the rise. Luteolin has a certain protective effect on myocardium. Therefore, this study focuses on whether luteolin can protect IRI in rats with myocardial infarction. A myocardial infarction rat model was prepared and the isolated heart was treated to induce cardiac ischemia-reperfusion injury. British biodegradable packaging company (BIOPAC) biological signal collector detects myocardial indicators; semi-automatic biochemical analyzer detects myocardial infarct size; hematoxylin-eosin (HE) staining observes pathological changes along with analysis of the levels of ERK, JNK, and Caspase-3 and proliferation and apoptosis of myocardial cells. Luteolin can improve the myocardial index level of rats with myocardial infarction and increase survival rate; the rats in luteolin group have the smallest myocardial infarction area, and the myocardial tissue is tightly arranged, the myocardial collagen is significantly reduced, and the myocardial injury index is significantly reduced. Luteolin inhibited the proliferation, migration and apoptosis of cardiomyocytes. Caspase-3, ERK, and JNK expression in the ERK/JNK agonist group was the most obvious. Their levels were highest in the luteolin+ERK/JNK agonist group (vs. other groups, P <0.05), which was higher than ERK/JNK agonist group. Luteolin can inhibit Caspase-3 expression by activating ERK/JNK signaling pathway, thereby reducing myocardial injury.