Liu Shengzhong, He Ying, Shi Jun, Liu Lulu, Ma Hao, He Li, Guo Yingqiang
Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Chengdu, P.R. China; Cardiac Surgery Center, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, P.R. China.
Psychosomatic Medicine Center, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, P.R. China.
Transplant Proc. 2019 Jul-Aug;51(6):2060-2065. doi: 10.1016/j.transproceed.2019.04.039.
To explore the protective effect and underlying mechanism of allicin (ALC) on myocardial ischemia reperfusion (MI/R) injury in rats.
The model of MI/R injury in rats was induced by ligating the left anterior descending branch of the coronary artery. Thirty male Sprague-Dawley rats were randomly divided into 3 equal groups (n = 10): sham group, MI/R injury group, and ALC precondition group. Enzyme-linked immunosorbent assay was used to examine the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the rats' serum. Hematoxylin and eosin staining was used to observe the myocardial pathologic morphology. A physiological recorder was used to measure cardiac systolic and diastolic function. Western blot analysis was used for detecting the expression of p38 and p-p38 in myocardium. The content of malondialdehyde and the activity of superoxide dismutase, catalase, and glutathione peroxidase in myocardium were examined by automatic analysis with the thiobarbituric acid chromogenic and dinitrobenzoic acid methods, respectively.
ALC can significantly decrease the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the serum and reduce the myocardial pathologic injury and the expression of malondialdehyde and p-p38 in myocardial tissue. Moreover, ALC can upregulate the activity of superoxide dismutase, catalase, and glutathione peroxidase and improve myocardial systolic and diastolic function with no influence on the expression of p38.
ALC can protect rats against MI/R injury by suppressing inflammation and oxidative stress. The mechanism is associated with alleviating the activation of p38 signaling.
探讨大蒜素（ALC）对大鼠心肌缺血再灌注（MI/R）损伤的保护作用及潜在机制。
通过结扎冠状动脉左前降支诱导大鼠MI/R损伤模型。30只雄性Sprague-Dawley大鼠随机分为3组，每组10只：假手术组、MI/R损伤组和ALC预处理组。采用酶联免疫吸附测定法检测大鼠血清中心肌肌钙蛋白I、肌酸激酶同工酶MB、白细胞介素-6、肿瘤坏死因子-α和白细胞介素-8的表达。采用苏木精-伊红染色观察心肌病理形态。使用生理记录仪测量心脏收缩和舒张功能。采用蛋白质免疫印迹分析检测心肌中p38和磷酸化p38的表达。分别采用硫代巴比妥酸显色法和二硝基苯甲酸法自动分析检测心肌中丙二醛含量以及超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性。
ALC可显著降低血清中心肌肌钙蛋白I、肌酸激酶同工酶MB、白细胞介素-6、肿瘤坏死因子-α和白细胞介素-8的表达，减轻心肌病理损伤以及心肌组织中丙二醛和磷酸化p38的表达。此外，ALC可上调超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性，改善心肌收缩和舒张功能，且对p38的表达无影响。
ALC可通过抑制炎症和氧化应激保护大鼠免受MI/R损伤。其机制与减轻p38信号通路的激活有关。
