Allicin attenuates myocardial apoptosis, inflammation and mitochondrial injury during hypoxia-reoxygenation: an in vitro study

BMC Cardiovascular Disorders

Peng Yang¹  Mengru Liu²  Tong Gao²  Xinyi Deng³  Xianlun Li⁴ 

[1] Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing, China;Graduate School, Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China;Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing, China;Peking University China-Japan Friendship School of Clinical Medicine, 2 East Yinghuayuan Street, Hepingli, 100029, Beijing, China;Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing, China;Peking University China-Japan Friendship School of Clinical Medicine, 2 East Yinghuayuan Street, Hepingli, 100029, Beijing, China;Graduate School, Peking Union Medical College and Chinese Academy of Medical Sciences, 100730, Beijing, China;Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing, China;

关键词: Myocardial ischemia–reperfusion;    Allicin;    Cardiomyocytes;    Apoptosis;    Inflammation;    Mitochondrial injury;   

DOI  :  10.1186/s12872-021-01918-6

来源: Springer

【 摘 要 】

BackgroundMyocardial 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.MethodsWe 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).ResultsAfter 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.ConclusionsThese 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.

【 授权许可】

CC BY