| Objective: to explore the protective effect and mechanisms of anti-myocardial ischemia of ginsenoside Re, in order to find safe and effective drug prevention and treatment of anti-myocardial ischemia and to provide experimental basis.Methods: The ligation of the left anterior descending coronary artery (LAD) in rats for 6h to establish the model of myocardial ischemia in vivo. The standardⅡ-lead electrocardiogram detected the HR continuously by the needle electrode inserting under the hypodermis of limbs. the cardio hemodynamics was monitored through place the pip in the femoral artery to detect the SBP, DBP and place the pip in left ventricle to detect LVSP,±dp/dtmax; the effect of ginsenoside Re on malondialdehyde (MDA) and superoxide dismutase (SOD) were measured; We detected the inflammatory cytokines of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) by radioimmunoassay; plasma levels of PGI2 and TXA2 were measured by radioimmunoassay. Some cardiac ischemic myocardium apical specimens were examined by transmission electron microscope.Results: The Ginsenoside Re can improve systolic and diastolic function in ischemic myocardium. It showed that Ginsenoside Re could improve the heart hemodynamics after being myocardial ischemia and increase the supplementation of blood of cardiac muscle. Compared with the model group, Re treatment Group can significantly lower serum MDA of coronary artery ligation rats while serum SOD activity can also markedly improved. Compared with the model group, Re treatment group can decrease the levels of IL-1βand TNF-αsignificantly. Were detected the change of TXA2 and PGI2 levels by immunohistochemistry; compared with the model group, Re treatment group are able to significantly lower plasma level of TXA2 and increase plasma level of PGI2 and the ratio of PGI2/TXA2. It can significantly inhibit the increase of vasoconstrictor substances to maintain PGI2/TXA2 physiological balance and help expand blood vessels, increasing myocardial blood supply. Myocardial histopathological observation: the model group: matrix swelling, focal myofilament dissolution,fracture, myofibrils disorder, nucleus was deformed, nuclear chromatin condensation and margination, mitochondria increase swelling size and have more vacuoles formation, the nucleus cavity-like change. Myocardial ultrastructure changes in Re treatment group were mild, sarcoplasmic edema slightly; myofilaments was arranged regularly, the bands of the sarcomere is clear; myofibril relaxation, a loose arrangement of local myofilaments; the mitochondria between myofilaments was increased slightly swollen.Conclusion: 1. Ginsenoside Re can significantly improve hemodynamic parameters in anesthetized rats, improving cardiac contractile function, indicating that its protective effect on ischemic myocardium. 2. Ginsenoside Re can reduce the expression of inflammatory cytokines TNF-αand IL-1β, reducing inflammation of myocardial tissue damage 3. Ginsenoside Re can improve superoxide dismutase activity of the endothelial cells of hypoxia, reducing lipid peroxidation, reducing the degree of myocardial cell injury. 4. Ginsenoside Re can significantly reduce the plasma levels of TXA2 and increase in plasma PGI2 level and the ratio of PGI2/TXA2 on the rats of acute myocardial infarction. It showed that can significantly inhibit the increase in vasoconstrictor substances to maintain PGI2/TXA2 physiological balance, and help expand blood vessels, increasing myocardial blood supply. 5. Ginsenoside Re can improve the ultrastructural changes of myocardial ischemia.
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