EGCG 通过降低心肌细胞内 Ca2+ 和增加 TnT 水平减少 I/R 和 MIRI 大鼠的心肌梗死。
EGCG decreases myocardial infarction in both I/R and MIRI rats through reducing intracellular Ca2+ and increasing TnT levels in cardiomyocytes.
机构信息
Department of Cardiovascular Medicine, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), China.
出版信息
Adv Clin Exp Med. 2021 Jun;30(6):607-616. doi: 10.17219/acem/134021.
BACKGROUND
Myocardial ischemia/reperfusion injury (MIRI) usually induces serious health problems.
OBJECTIVES
This study attempted to explore protective effects of (-)-epigallocatechin-3-gallate (EGCG) on MIRI and the associated mechanism.
MATERIAL AND METHODS
Ischemia/reperfusion of an isolated rat heart (I/R model) and the MIRI model were used in this study. Myocardial infarction was measured with staining with 2,3,5-triphenyltetrazolium chloride (TTC). Ca2+ and troponin T (TnT) concentrations in coronary perfusion fluid were evaluated using the chromatometry method. Ca2+ concentration in cardiomyocytes was determined with detecting Ca2+ fluorescence intensity. The ultrastructure of cardiomyocytes was observed using transmission electron microscopy (TEM). β-nicotinamide adenine dinucleotide (NAD+) of cardiomyocytes was also determined.
RESULTS
The EGCG (I/R+EGCG) significantly reduced myocardial infarction size of isolated rat heart compared to I/R rats (p < 0.05), remarkably increased Ca2+ and decreased TnT concentrations in coronary perfusion fluid of I/R rats compared to the I/R model (p < 0.05), as well as markedly decreased intracellular Ca2+ concentration and promoted NAD+ concentration in cardiomyocytes compared to I/R rats (p < 0.05). It also obviously maintained the mitochondrial structure in cardiomyocytes of I/R rats and improved the ultrastructure of cardiomyocytes of MIRI rats. Lonidamine (LND) treatment (I/R+EGCG+LND group) significantly blocked the effects of EGCG on I/R injury compared to the I/R+EGCG group (p < 0.05). The EGCG (MIRI+EGCG) significantly decreased myocardial infarction size compared to MIRI rats (p < 0.05) and remarkably enhanced Ca2+ and reduced TnT concentrations in the pulmonary artery compared to that of MIRI rats (p < 0.05).
CONCLUSIONS
The EGCG decreased myocardial infarction size in both I/R models and MIRI models by reducing intracellular Ca2+ concentration, increasing TnT concentration, promoting NAD+ concentration, and improving the ultrastructure of cardiomyocytes.
背景
心肌缺血再灌注损伤（MIRI）通常会引发严重的健康问题。
目的
本研究试图探讨表没食子儿茶素没食子酸酯（EGCG）对 MIRI 的保护作用及其相关机制。
材料和方法
本研究采用离体大鼠心脏缺血/再灌注（I/R 模型）和 MIRI 模型。用 2,3,5-三苯基氯化四氮唑（TTC）染色测量心肌梗死。用色谱法评估冠状动脉灌流液中的 Ca2+和肌钙蛋白 T（TnT）浓度。用检测 Ca2+荧光强度的方法测定心肌细胞内 Ca2+浓度。用透射电子显微镜（TEM）观察心肌细胞的超微结构。还测定了心肌细胞中的β-烟酰胺腺嘌呤二核苷酸（NAD+）。
结果
与 I/R 大鼠相比，EGCG（I/R+EGCG）显著降低了离体大鼠心脏的心肌梗死面积（p<0.05），显著增加了 I/R 大鼠冠状动脉灌流液中的 Ca2+浓度，降低了 TnT 浓度（p<0.05），同时显著降低了心肌细胞内 Ca2+浓度，促进了 NAD+浓度（p<0.05）。与 I/R 大鼠相比，它还明显维持了 I/R 大鼠心肌细胞的线粒体结构，改善了 MIRI 大鼠的心肌细胞超微结构。用 Lonidamine（LND）处理（I/R+EGCG+LND 组）与 I/R+EGCG 组相比，明显阻断了 EGCG 对 I/R 损伤的作用（p<0.05）。与 MIRI 大鼠相比，EGCG（MIRI+EGCG）显著降低了心肌梗死面积（p<0.05），显著增加了肺动脉中的 Ca2+浓度，降低了 TnT 浓度（p<0.05）。
结论
EGCG 通过降低细胞内 Ca2+浓度、增加 TnT 浓度、促进 NAD+浓度和改善心肌细胞超微结构，减少 I/R 模型和 MIRI 模型中的心肌梗死面积。
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