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
心肌缺血-再灌注(IR)损伤是由于最初流向心脏的血流量减少，使其无法获得足够的氧气，然后通过闭塞的冠状动脉开放而恢复血流，从而产生矛盾的有害影响所造成的损害。寻找预防IR的新疗法是至关重要的。大蒜素是从大蒜中分离出来的一种化合物，具有预防和治疗各种疾病的能力，对心肌也有保护作用。因此，本研究旨在探讨大蒜素对心肌细胞缺血再灌注损伤的保护作用。我们建立了原代猪心肌细胞缺氧-复氧(HR)模型，模拟心肌缺血再灌注损伤。原代培养的猪心肌细胞取自1日龄小型麝香猪。经过至少2~3h的适应后，选择条件良好的心肌细胞，随机分为对照组(常氧5h)、HR组(缺氧2h/复氧3h)、HR + 大蒜素组(缺氧/复氧 + 大蒜素治疗)。在缺氧/复氧诱导后，大蒜素处理可提高细胞存活率。与HR组比较，大蒜素处理组细胞凋亡率由13.5 ± 1.2%降至6.11 ± 0.15%(p <； 0.05)，细胞凋亡相关蛋白表达受到调控，Bax、裂解caspase-3和胞浆细胞色素C表达减少，Bcl2表达增加(p + <； 0.01)。大蒜素治疗可下调促炎细胞因子，如白介素6和肿瘤坏死因子α(p <； 0.01)。此外，它还能显著减少细胞内活性氧的产生(p 和lt； )，并减少线粒体膜电位的损失(p 和lt； 0.01)。此外，大蒜素还上调了PPARγ共激活因子-1α和内皮型一氧化氮合酶的表达(p 和 均为0.01)，下调了内皮素-1、缺氧诱导因子-1α和转化生长因子β的表达(均为p 和 0.01)。这些结果提示，大蒜素通过减少细胞凋亡、炎症和线粒体损伤来保护心肌细胞免受HR损伤，从而为其在治疗心肌缺血再灌注中的潜在应用提供了依据。网上版载有补充材料，可在10.1186/s12872-021-01918-6查阅。
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.