Abstract
Objective: To investigate whether cardiac stem cells (CSCs) can attenuate oxidative stress and improve sympathetic remodeling in rats following myocardial infarction (MI). Methods: Sprague-Dawley rats were randomly divided into three groups: 1) MI with CSCs transplantation (CSCs group, n=15); 2) MI control (Control group, n=15); 3) sham control group (Sham group, n=10). Two weeks after surgery, the animals were subjected to intramyocardial injection. Four weeks after injection, left ventricular function, level of oxidative stress, cardiac nerve sprouting and nerve growth factor (NGF) expression were determined. Results: At 4 weeks after intramyocardial injection, fractional shortening (FS) and left ventricular ejection fraction (LVEF) markedly decreased in CSCs and control groups. However, systolic function were partly preserved in CSCs group compared with control group (P<0.01). The myocardial malondialdehyde (MDA) content, MDA/Superoxide Dismutase (SOD) ratio, NGF expression and density of tyrosine hydroxylase (TH)-positive nerve in peri-infarct zone was significantly increased in the control group and CSCs group than the sham group (all P<0.01). However, all of these valuables were decreased in CSCs group when compared with control group (all P<0.01 except for NGF expression P< 0.05). Furthermore, a positive correlation was observed between the degree of sympathetic remodeling and the level of MDA/SOD ratio (r=0.86, R2=0.75). Conclusion: CSCs suppressed sympathetic remodeling after MI probably via attenuated oxidative stress and downregulated NGF expression, which in turn leads to a promising treatment for SCD post MI.
Highlights
Sudden cardiac death (SCD) is one of the most common and often the first manifestation of coronary heart disease and account for 50% of coronary heart disease deaths and 15% to 20% of all deaths in developed countries [1]
Two weeks after myocardial infarction (MI) induction, fractional shortening (FS) and left ventricular ejection fraction (LVEF) were markedly decreased when compared with baseline, which indicates the development of significant left ventricular dysfunction post MI; both of FS and LVEF were virtually indistinguishable between the control and cardiac stem cells (CSCs) groups, which demonstrates that the similar degree of left ventricular systolic functional deterioration at the time of treatment
In the control group, FS and LVEF represented downward trend but no significant change during the following 4 weeks (P > 0.05); in contrast, at 6 weeks, FS and LVEF of CSCs group were partly preserved when compared with 2 weeks (P
Summary
Sudden cardiac death (SCD) is one of the most common and often the first manifestation of coronary heart disease and account for 50% of coronary heart disease deaths and 15% to 20% of all deaths in developed countries [1]. Life-threatening ventricular arrhythmias occur often in chronic myocardial infarction (MI) but the mechanism remains unclear. Studies have shown that sympathetic remodeling post MI plays an important role in life-threatening ventricular arrhythmias and even SCD [2,3,4]. Laboratory experiments and recent clinical trials suggest that cell-based therapies for MI can improve cardiac function. Resident cardiac stem cells (CSCs) appears as a promising stem cell because of the ability of differentiating into cardiomyocytes, endothelial cells, vascular smooth muscle cells, and fibroblasts [9, 10], demonstrating improvement of left ventricular function. Our previous study has shown that rats post MI treated with CSCs improved cardiac electrophysiological stability and ventricular fibrillation threshold [11]
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