Academic Journal
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
| العنوان: | 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 |
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| المؤلفون: | Liu, Hanqing, Liu, Wei, Qiu, Huiliang, Zou, Dezhi, Cai, Huayang, Chen, Qiuxiong, Zheng, Chaoyang, Xu, Danping |
| المساهمون: | Guangzhou Science and Technology Plan project, Guangdong Provincial Science and Technology Plan, Innovation Specific Project in Key Areas from Guangdong Branch Institute of China Academy of Chinese Medical Sciences |
| المصدر: | Naunyn-Schmiedeberg's Archives of Pharmacology ; volume 393, issue 8, page 1527-1539 ; ISSN 0028-1298 1432-1912 |
| بيانات النشر: | Springer Science and Business Media LLC |
| سنة النشر: | 2019 |
| الوصف: | 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. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1007/s00210-019-01755-7 |
| DOI: | 10.1007/s00210-019-01755-7.pdf |
| DOI: | 10.1007/s00210-019-01755-7/fulltext.html |
| الاتاحة: | http://dx.doi.org/10.1007/s00210-019-01755-7 https://link.springer.com/content/pdf/10.1007/s00210-019-01755-7.pdf https://link.springer.com/article/10.1007/s00210-019-01755-7/fulltext.html |
| Rights: | https://creativecommons.org/licenses/by/4.0 ; https://creativecommons.org/licenses/by/4.0 |
| رقم الانضمام: | edsbas.C63DC775 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1007/s00210-019-01755-7 |
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