Abstract
Through in vitro experiments, the paper investigated whether Lycopene can mitigate cardiac ischemia/reperfusion injury, and further explored whether the underlying mechanism works by inhibiting the opening of MPTP.A hypoxia-reoxygenation model was established. CCK8 was employed to determine the viability of H9c2 cardiomyocytes. LDH was used to determine the degree of damage of H9c2 cardiomyocytes. Trypan blue staining was applied to determine the survival rate of H9c2 cardiomyocytes. Flow cytometry was used to determine the apoptosis rate of H9c2 cardiomyocytes. Rhodamine 123 staining method was applied to evaluate the changes of mitochondrial membrane potential of H9c2 cardiomyocytes. Western blot was employed to determine the protein expressions of related factors of MPTP downstream apoptosis pathway in H9c2 cardiomyocytes. Calcium induction method was used to evaluate the opening degree of MPTP of H9c2 cardiomyocytes. Western blot was applied to determine the protein expressions of the related factors regulating MPTP opening in H9c2 cardiomyocytes.The vitality of H9c2 cardiomyocytes in the Lycopene group was significantly improved, the LDH activity was significantly reduced, and the cell survival rate was significantly improved. The apoptosis rate was significantly reduced, and the membrane potential decreased significantly. The expression levels of Bax, cytochrome C, APAF-1, caspase 9 and caspase-3 proteins were significantly reduced. The sensitivity of MPTP opening was significantly decreased. Lycopene can effectively alleviate the hypoxia/reoxygenation injury of H9c2 cardiomyocytes. By up-regulating Bcl-2 and down-regulating Bax, Lycopene can inhibit the opening of mitochondrial MPTP and the activation of downstream apoptotic pathways, thereby reducing apoptosis.
Highlights
The heart is the most energy-consuming organ in the human body, but the concentration of ATP in myocardial cells is relatively low, which means that myocardial cells must continuously synthesize ATP to maintain normal diastolic and contractile functions
Our research is to explore whether Lycopene can mitigate cardiac ischemia/reperfusion injury, and to further explore whether its underlying mechanism plays a role by inhibiting the opening of mitochondrial permeability transition pore (MPTP)
Lycopene on Ischemia-reperfusion Myocardium in which the cells were grown in an incubator, without receiving sugar-free Earle’s medium replacement; B, the H/R group, in which the cells received sugar-free Earle’s medium and normal medium in sequence, meaning that the cells were treated with hypoxia for 12 h and reoxygenation for 1 h respectively; C, the low-dose drug group
Summary
The heart is the most energy-consuming organ in the human body, but the concentration of ATP in myocardial cells is relatively low, which means that myocardial cells must continuously synthesize ATP to maintain normal diastolic and contractile functions. Cardiomyocytes contain a large number of mitochondria, a double-layer membrane-coated organelle that exists in most cells. It is the main structure for energy production in cells and the main place for cells to carry out aerobic respiration. Mitochondrial injury is the main pathogenesis that causes myocardial ischemia/reperfusion injury, which in turn leads to myocardial death, apoptosis and contractile failure. Mitochondrial dysfunction is a determinant of myocardial ischemia/reperfusion injury. Studies have found that autologous mitochondria transplantation, in which a person’s autologous healthy mitochondria is delivered to the ischemic area of damaged mitochondria through mitochondria in coronary arteries, can significantly improve myocardial function (Giorgio et al, 2018; Shin et al, 2019; Chiva-Blanch & Badimon, 2017; Espinosa-Moncada et al, 2018; Vetrani et al, 2018)
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