Abstract
Salvianolic acid B (Sal B) has a significant protective effect on myocardial ischaemia-reperfusion (I/R) injury. Therefore, the aims of this study were to determine the effects of Sal B on myocardial ischaemic-reperfusion (I/R) injury in rats and to explore whether its underlying mechanism of cardioprotection occurs through activating the expression of the phosphoinositide 3-kinase/protein, kinase B (PI3K/Akt) and inhibiting the expression of high mobility group protein 1 (HMGB1). Ninety Sprague-Dawley rats were randomized into five groups: group 1 (sham-operated), group 2 (myocardial I/R), group 3 (low dose of Sal B+I/R), group 4 (high dose of Sal B+I/R), and group 5 (high dose of Sal B+I/R+LY294002, which is a specific PI3k inhibitor). All I/R rats received 30 min myocardial ischaemia followed by 24-h reperfusion. Cardiac function, infarct size, myocardial injury marker levels, inflammatory response and cardiomyocyte apoptosis as well as Bcl-2, Bax, P-Akt, HMGB1 and TLR4 expression were measured. In the current study, Sal B significantly ameliorated myocardial I/R injury in a dose-dependent manner, ameliorated cardiac function, reduced myocardial infarction size, decreased myocardial injury marker expression, decreased inflammatory responses, reduced apoptosis, activated PI3K/Akt expression and inhibited HMGB1 expression. However, all effects of Sal B were significantly reversed by LY294002. Overall, the present study indicated that Sal B attenuated myocardial I/R injury by activating PI3K/Akt and inhibiting the release of HMGB1 in rats.
Highlights
Coronary heart disease is a leading cause of death associated with cardiovascular disease
The levels of L-Lactate dehydrogenase (L-LDH), CK-MB, tumour necrosis factor-α (TNF-α), IL-18, IL1β and HMGB1 in the ischaemia and reperfusion (I/R) group treated with Salvianolic acid B (Sal B) (60 mg/kg) were significantly abolished by LY294002 treatment (P < 0.05). These results demonstrated that Sal B had a protective effect against myocardial I/R injury and inflammatory response, while LY294002 had a partial reversal effect on myocardial I/R injury (P < 0.05)
After treatment with Sal B, the expression of Bcl-2 and the ratio of Bcl-2/Bax significantly increased and the expression of Bax decreased (P < 0.05). These results showed that Sal B could effectively reduce cardiomyocyte apoptosis
Summary
Coronary heart disease is a leading cause of death associated with cardiovascular disease. Acute myocardial infarction (AMI)-associated mortality and morbidity are common worldwide (Frank et al 2012). Myocardial reperfusion is the preferred treatment for AMI in most clinical settings (Binder et al 2015). The rapid restoration of blood flow is a critical. Hanqing Liu and Wei Liu contributed to this work. Hanqing Liu and Wei Liu should be considered to share first authorship. The mechanism of myocardial I/R injury is very complex. There are numerous causes of myocardial I/R injury, such as inflammation, apoptosis, mitochondrial dysfunction and oxidative stress (Braunersreuther et al 2013; Zhu et al 2015; Li et al 2016a, b, Wang, Han and Jia 2018)
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