Abstract
BackgroundOur previous studies suggested that deoxyschizandrin (DSD) and schisantherin A (STA) may have cardioprotective effects, but information in this regard is lacking. Therefore, we explored the protective role of DSD and STA in myocardial ischemia–reperfusion (I/R) injury.Methodology/Principal FindingsAnesthetized male rats were treated once with DSD and STA (each 40 µmol/kg) through the tail vein after 45 min of ischemia, followed by 2-h reperfusion. Cardiac function, infarct size, biochemical markers, histopathology and apoptosis were measured and mRNA expression of gp91phox in myocardial tissue assessed by RT-PCR. Neonatal rat cardiomyocytes were pretreated with DSD and STA and then damaged by H2O2. Cell apoptosis was tested by a flow cytometric assay. Compared with the I/R group: (i) DSD and STA could significantly reduce the abnormalities of LVSP, LVEDP, ±dp/dtmax and arrhythmias, thereby showing their protective roles in cardiac function; (ii) DSD and STA could significantly attenuate the infarct size and MDA release while increasing SOD activity, suggesting a role in reducing myocardial injury; (iii) tissue morphology and myocardial textual analysis revealed that DSD and STA mitigated changes in myocardial histopathology; (iv) DSD and STA decreased apoptosis (33.56±2.58% to 10.28±2.80% and 10.98±1.99%, respectively) and caspase-3 activity in the myocardium (0.62±0.02 OD/mg to 0.38±0.02 OD/mg and 0.32±0.02 OD/mg, respectively), showing their protective effects upon cardiomyocytes; and (v) DSD and STA had similar protective effects on I/R injury as those seen with the positive control metoprolol. In vitro, DSD and STA could significantly decrease the apoptosis of neonatal cardiomyocytes.Conclusions/SignificanceThese data suggest that DSD and STA can protect against myocardial I/R injury. The underlining mechanism may be related to their role in inhibiting cardiomyocyte apoptosis.
Highlights
Acute myocardial infarction is due to the death of myocardial cells caused by thrombotic occlusion of the coronary artery
Every drug tested caused a decrease in the prevalence and duration of Ventricular fibrillation (VF) as well as the arrhythmia score compared with the I/R group during the stabilization and reperfusion phases (P,0.01)
When compared with each other, the arrhythmia score was lower in the Effect on myocardial infarct size AAR/left ventricle (LV) was comparable among all groups (Figure 3B), averaging between 35% and 40%
Summary
Acute myocardial infarction is due to the death of myocardial cells caused by thrombotic occlusion of the coronary artery. Acute myocardial infarction is the leading cause of death in human cardiovascular disease. Mitigating myocardial ischemia–reperfusion (I/R) injury is an important means for the treatment of ischemic heart disease [4]. A recent study demonstrated that Fructus Schisandrae was the anti-oxidant component herb in a Chinese medicinal formula called ‘‘Sheng Mai San’’ which is commonly used for the treatment of coronary heart disease [6]. Investigations revealed that lignans from Schisandra, including deoxyshisandrin (DSD) and schisantherin A (STA), are the principal active constituents of Fructus Schisandrae, and that they have liver-protective, anti-tumor and anti-oxidant activities [7]. We explored the protective role of DSD and STA in myocardial ischemia–reperfusion (I/R) injury
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