Allicin attenuates myocardial apoptosis, inflammation and mitochondrial injury during hypoxia-reoxygenation: an in vitro study.
Allicin attenuates myocardial apoptosis, inflammation and mitochondrial injury during hypoxia-reoxygenation: an in vitro study.
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大蒜素减轻缺氧-复氧过程中的心肌细胞凋亡、炎症和线粒体损伤:一项体外研究
DOI:
10.1186/s12872-021-01918-6
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发表时间:
2021-04-21
影响因子:
2.1
通讯作者:
Li X
中科院分区:
文献类型:
--
作者:
Deng X;Yang P;Gao T;Liu M;Li X
Myocardial ischemia–reperfusion (IR) injury is a damage due to an initial reduction in blood flow to the heart, preventing it from receiving enough oxygen, and subsequent restoration of blood flow through the opening of an occluded coronary artery producing paradoxical harmful effects. The finding of new therapies to prevent IR is of utmost importance. Allicin is a compound isolated from garlic having the ability to prevent and cure different diseases, and a protective effect on the myocardium was also demonstrated. Therefore, the aim of this study was to evaluate the in vitro protective effect of Allicin against myocardial IR injury on cardiomyocytes. We established an in vitro hypoxia-reoxygenation (HR) model of primary porcine cardiomyocytes to simulate myocardial IR injury. Primary porcine cardiomyocytes were extracted from Mini-musk swines (1 day old). After a period of adaptation of at least 2–3 days, cardiomyocytes in good condition were selected and randomly divided into control group (normal oxygen for 5 h), HR group (2 h of hypoxia/3 h of reoxygenation), and HR + Allicin group (hypoxia/reoxygenation + Allicin treatment). After the induction of hypoxia/reoxygenation, Allicin treatment enhanced the cell viability. Moreover, Allicin treatment resulted in a reduction of apoptosis from 13.5 ± 1.2% to 6.11 ± 0.15% compared with the HR group (p < 0.05), and the apoptosis related proteins were regulated as well, with a decreased expression of Bax, cleaved caspase-3 and cytosolic cytochrome C and an increase in Bcl-2 expression in the HR + Allicin group (all p < 0.01). Pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor alpha were down-regulated by the treatment with Allicin (both p < 0.01). In addition, it significantly decreased intracellular reactive oxygen species generation (p < 0.01) and reduced the loss of mitochondrial membrane potential (p < 0.01). Furthermore, the expression of PPARγ coactivator-1α and endothelial nitric oxide synthase was up-regulated (both p < 0.01), while the expression of Endothelin-1, hypoxia inducing factor-1α and transforming growth factor beta was down-regulated (all p < 0.01) by Allicin treatment. These results suggested that Allicin protected the cardiomyocytes against HR damage by reducing apoptosis, inflammation and mitochondrial injury, thus providing a basis for its potential use in the treatment of myocardial IR. The online version contains supplementary material available at 10.1186/s12872-021-01918-6.
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影响因子:
4.2
作者:
Varshney, Ravi;Budoff, Matthew J.
通讯作者:
Budoff, Matthew J.
DOI:
10.3109/10731199.2011.649187
发表时间:
2012-08-01
期刊:
ARTIFICIAL CELLS BLOOD SUBSTITUTES AND BIOTECHNOLOGY
影响因子:
--
作者:
Yang Peng;Li Jiahui;Li Xianlun
通讯作者:
Li Xianlun
影响因子:
2.9
作者:
Yang Peng;Li Jia-hui;Li Xian-lun
通讯作者:
Li Xian-lun
影响因子:
20.1
作者:
Bagai, Akshay;Dangas, George D.;Granger, Christopher B.
通讯作者:
Granger, Christopher B.
影响因子:
37.8
作者:
Ramzy, Danny;Rao, Vivek;Ross, Heather J.
通讯作者:
Ross, Heather J.