Abstract
Objective Ischemic heart disease (IHD) has always been the focus of attention of many researchers in cardiovascular disease, and its pathogenesis is also very complicated. Ferroptosis may be involved in the occurrence and development of IHD. Methods First, primary cardiomyocytes were treated with H2O2 to simulate the IHD in vitro model. After pretreatment with different concentrations of ferrostatin-1, cell survival rate was detected by MTT method, cell apoptosis was detected by TUNEL staining and flow cytometry, and the expression of oxidative stress, ferroptosis, and related molecules of Nrf2/ARE pathway was detected by Western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR). Results The mortality of primary cardiomyocytes in the H2O2 group was obviously increased. Ferrostatin-1 treatment can effectively inhibit cell death, improve antioxidant enzyme activity, inhibit the expression of ferroptosis-related molecules, and activate Nrf2/ARE pathway expression. Conclusion Ferroptosis-specific inhibitor ferrostatin-1 relieves H2O2-induced redox imbalance in primary cardiomyocytes through the Nrf2/ARE pathway, inhibits ferroptosis, and thereby slows cardiomyocyte death.
Highlights
Ischemic heart disease (IHD) is the most common cause of health problems and heart failure in the world
We examined the effect of different ferrostatin-1 concentrations on the survival rate of primary cardiomyocytes using the MTT kit (Figure 1(b))
The results showed that after ferrostatin-1 was applied to primary cardiomyocytes at a concentration range of 3 μM–12 μM for 12 hours, there was no significant change in cell survival compared with the normal group, indicating that ferrostatin-1 had no significant effect on the growth of primary cardiomyocytes at this dose range
Summary
Ischemic heart disease (IHD) is the most common cause of health problems and heart failure in the world. As a common chronic disease, IHD can often cause myocardial ischemia, hypoxia, and even necrosis, posing a serious threat to human health [1]. An important pathophysiological mechanism of IHD is oxidative stress (OS) injury. In the occurrence of IHD, cardiomyocytes produce a large number of oxygen free radicals, and at the same time, the activity of antioxidant enzymes in the cells is reduced, resulting in lipid peroxidation on the cell membrane, the change of membrane permeability, and the destruction of cell function and structure and inducing the occurrence of cell death [5]. With the increase of the global aging population, IHD has become one of today’s serious social problems. The research on the pathogenesis, prevention, and treatment of IHD has profound significance
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