Affiliation:
1. Department of Cardiology, Affiliated Hospital of Nanjing University of Chinese Medicine (Jiangsu Province Hospital of Chinese Medicine), Nanjing, Jiangsu, 210023, China
2. Department of Cardiology, Xuzhou Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu, 221010, China
Abstract
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.
Publisher
American Scientific Publishers
Subject
General Materials Science