Allicin Attenuates Myocardial Apoptosis, Inflammation and Mitochondrial Injury during ischemia-reperfusion: An In Vitro Study
Allicin Attenuates Myocardial Apoptosis, Inflammation and Mitochondrial Injury during ischemia-reperfusion: An In Vitro Study
复制标题
大蒜素减轻缺血再灌注期间的心肌细胞凋亡、炎症和线粒体损伤：一项体外研究
DOI：
--
复制
发表时间：
--
影响因子：
2.1
通讯作者：
Xianlun Li
中科院分区：
文献类型：
--
作者：
Xinyi Deng;Peng Yang;Tong Gao;Mengru Liu;Xianlun Li
背景：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的损害。因此，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，本研究旨在评价大蒜素对心肌细胞IR损伤的保护作用。方法：原代培养的猪心肌细胞取自1日龄小型麝香猪。结果：与IR组比较，IR组心肌细胞凋亡率由27.9%±5.9%降至9.4%±0.7%(p<；0.05)，细胞凋亡相关蛋白表达下调，Bax、caspase-3和细胞色素C表达减少，细胞色素C表达增强(P均<0.01)。大蒜素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<；0.01)，减少线粒体膜电位的损失(p<；0.01)。此外，大蒜素可上调PPARγ共激活因子-1α和内皮型一氧化氮合酶的表达(P均<0.01)，下调内皮素-1、缺氧诱导因子-1α和转化生长因子β的表达(均P<0.01)。结论：大蒜素可能通过减少心肌细胞的凋亡、炎症和线粒体损伤而保护心肌细胞免受IR损伤。
Background: 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. Therefore, 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..Methods: 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, IR group, and IR+Allicin group..Results: After the induction of IR, Allicin treatment resulted in a reduction of apoptosis from 27.9% ± 5.9% to 9.4% ± 0.7% compared with the IR group (p < 0.05), and the apoptosis related proteins were regulated as well, with a decreased expression of Bax, cleaved caspase-3 and cytochrome C and an increase in Bcl-2 expression in the IR+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..Conclusions: These results suggested that Allicin protected the cardiomyocytes against IR damage by reducing apoptosis, inflammation and mitochondrial injury.