Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway
- Naunyn Schmiedebergs Arch Pharmacol. 2020 Aug;393(8):1527-1539. doi: 10.1007/s00210-019-01755-7.
- 1. Cardiovascular Department, Guangzhou Hospital of integrated Traditional and West Medicine, Guangzhou, 510800, China.
- 2. Geriatrics Department, Tongde Hospital of Zhejiang Province, Hangzhou, 310012, Zhejiang, China.
- 3. Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
- 4. Emergency Department, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
- 5. Internal Medicine Department, Guangdong Provincial Hospital of Chinese Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
- 6. Cardiovascular Department, Guangdong Provincial Hospital of Chinese Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
- 7. Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. [email protected].
- 8. Cardiovascular Department, Guangdong Provincial Hospital of Chinese Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China. [email protected].
- 9. Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. [email protected].
- 10. Cardiovascular Department, Guangdong Provincial Hospital of Chinese Medicine, 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China. [email protected].
- 11. Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, 510006, China. [email protected].
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.