Abstract
Background/Aims Coronary microembolization- (CME-) induced myocardial injury and progressive cardiac dysfunction are mainly caused due to CME-induced myocardial local inflammatory response and myocardial apoptosis. Ligustrazine plays an important protective role in multiple cardiovascular diseases, but its role and the protection mechanism in CME is unclear. This study hypothesized that ligustrazine attenuates CME-induced myocardial injury in rats. This study also explored the mechanism underlying this attenuation. Methods Forty SD rats were randomly divided into CME group, ligustrazine group, ligustrazine+LY294002 (ligustrazine+LY) group, and sham group (ten rats in each). In each group, the cardiac function, apoptotic index, serum c-troponin I (cTnI) level, inflammation [interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α)], and oxidative stress [nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA)] were determined. Western blotting was used to detect the proteins which are present in the PI3K/Akt pathway. Results Ligustrazine improved cardiac dysfunction induced by CME, increased serum NO and SOD activities, and decreased the serum level in IL-1β, MDA, cTnI, and TNF-α. Moreover, ligustrazine inhibited myocardial apoptosis, which is perhaps caused by the upregulated Bcl-2, the downregulated cleaved caspase-3 and Bax, and the increased protein level in endothelial nitric oxide synthase and phosphorylated Akt. These effects, however, were reduced if ligustrazine was coadministered with LY294002. Conclusions Ligustrazine attenuates CME-induced myocardial injury. The effects associated with this attenuation may be achieved by activating the myocardium PI3K/Akt signaling pathway.
Highlights
A serious complication in distal microvascular embolism, coronary microembolization (CME), is normally attributed to the detachment of atherosclerotic plaque debris which occurs in percutaneous coronary intervention (PCI)
The data presented in this study demonstrated that ligustrazine could protect cardiac function in CME rats, which is associated with suppression of the damage and inflammatory cytokines which are triggered by oxidative stress
It is believed that inflammatory reaction and cardiomyocyte apoptosis in normal myocardial tissues around the microinfarction are associated with myocardial injury as well as the progressive cardiac dysfunction after CME [30, 31]
Summary
A serious complication in distal microvascular embolism, coronary microembolization (CME), is normally attributed to the detachment of atherosclerotic plaque debris which occurs in percutaneous coronary intervention (PCI). CME can reduce coronary and inotropic reserves and induce noreflow phenomenon and is considered to be an independent predictor for major cardiac adverse events and poor long-term prognosis [1–4]. Previous studies have shown that local myocardial inflammation caused by CME is the main cause of progressive cardiac dysfunction [9, 10]. Several animal studies have shown that the necrotic/apoptotic cardiomyocytes and the microembolic areas occur during the acute phase of CME [13, 14]. In cardiac systolic dysfunction induced by CME, cardiomyocyte apoptosis plays a key role and its suppression reduces CMEinduced myocardial injuries [15, 16]. Su et al [17] reported that cardiomyocyte apoptosis after CME in rats caused myocardial injury.
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