Zhao Meng-qiu, Tu Peng-cheng, Ren You-nan, Tao Shan-jun, Zheng Shu-guo
Zhong Yao Cai. 2016 Jul;39(7):1633-7.
To investigate the protective effect of sesamin on myocardial ischemia reperfusion injury in rats, and to study the possible mechanism.
50 SD rats were randomly divided into control group, sham operated group, model group, high-dose sesamin group( 160 mg / kg) and low-dose sesamin group( 80 mg / kg),with 10 rats in each group. Rats in sesamin groups were administered intragastrically with sesamin for 7 d. Then all rats except those in sham operated group were subjected to myocardial ischemia-myocardial ischemia reperfusion injury model by coronary artery ligation for 40 min and subsequent reperfusion for 120 min. Serum cardiac troponin Ⅰ( c TnⅠ) and lactate dehydrogenase( LDH),levels of total antioxidant capacity( TAOC) and nitric oxide( NO) in serum and myocardial tissues,Caspase-3 activity in myocardial tissues were detected by colorimetric assay. Cardiomyocyte apoptosis was evaluated by TUNEL assay. Phosphorylation level of endothelial nitric oxide synthase( eNOS) and Protein kinase B( Akt), protein expression of superoxide dismutase( SOD) in cardiac tissue were determined by Western blot.
Pretreatment with sesamin significantly ameliorated myocardial injury in rats which induced myocardial ischemia and reperfusion injury by reduced levels of serum c TnⅠand LDH( P <0. 05 or P < 0. 01). Supplementation with sesamin resulted in a significant increasing of total antioxidant capacity and NO level in serum and myocardial tissues and cardiomyocyte apoptosis( P < 0. 05 or P < 0. 01),and remarkable decrease the Caspase-3 activity in myocardial tissues and cardiomyocyte apoptosis( P < 0. 05 or P < 0. 01). Sesamin significantly up-regulated the protein expression of SOD in cardiac tissues, and the levels of phosphorylated eNOS and Akt increased notably( P < 0. 05 or P < 0. 01).
Pretreatment with sesamin effectively ameliorated myocardial ischemia reperfusion injury in rats, and the mechanism might be related to enhancing its antioxidant capacity and the activation of Akt / eNOS signaling pathway and subsequent increase of NO synthesis and suppression of cardiac myocyte apoptosis.
探讨芝麻素对大鼠心肌缺血再灌注损伤的保护作用，并研究其可能的机制。
将50只SD大鼠随机分为对照组、假手术组、模型组、高剂量芝麻素组（160mg/kg）和低剂量芝麻素组（80mg/kg），每组10只。芝麻素组大鼠灌胃给予芝麻素7天。然后，除假手术组大鼠外，其余大鼠均通过冠状动脉结扎40分钟并随后再灌注120分钟建立心肌缺血-心肌缺血再灌注损伤模型。采用比色法检测血清心肌肌钙蛋白Ⅰ（cTnⅠ）、乳酸脱氢酶（LDH）、血清和心肌组织中总抗氧化能力（TAOC）和一氧化氮（NO）水平、心肌组织中Caspase-3活性。通过TUNEL法评估心肌细胞凋亡。采用蛋白质印迹法检测心脏组织中内皮型一氧化氮合酶（eNOS）和蛋白激酶B（Akt）的磷酸化水平、超氧化物歧化酶（SOD）的蛋白表达。
芝麻素预处理可显著改善大鼠心肌缺血再灌注损伤，降低血清cTnⅠ和LDH水平（P<0.05或P<0.01）。补充芝麻素可显著提高血清和心肌组织中的总抗氧化能力和NO水平，并减少心肌细胞凋亡（P<0.05或P<0.01），同时显著降低心肌组织中Caspase-3活性和心肌细胞凋亡（P<0.05或P<0.01）。芝麻素可显著上调心脏组织中SOD的蛋白表达，eNOS和Akt的磷酸化水平显著升高（P<0.05或P<0.01）。
芝麻素预处理可有效改善大鼠心肌缺血再灌注损伤，其机制可能与增强抗氧化能力、激活Akt/eNOS信号通路、随后增加NO合成以及抑制心肌细胞凋亡有关。
