| 马晓玮,张小敏,刘 洁,侯 杰,陈娟娟.曲美他嗪对心肌梗死后心力衰竭大鼠炎症反应、氧化应激及心肌细胞自噬的影响[J].,2020,(17):3239-3242 |
| 曲美他嗪对心肌梗死后心力衰竭大鼠炎症反应、氧化应激及心肌细胞自噬的影响 |
| Effects of Trimetazidine on Inflammatory Response, Oxidative Stress and Autophagy of Cardiac Myocytes in Heart Failure Rats after Myocardial Infarction |
| 投稿时间：2020-04-23 修订日期：2020-05-19 |
| DOI：10.13241/j.cnki.pmb.2020.17.008 |
| 中文关键词: 心肌梗死 心力衰竭 曲美他嗪 炎症反应 氧化应激 心功能 心肌细胞自噬 |
| 英文关键词: Myocardial infarction Heart failure Trimetazidine Inflammatory response Oxidative stress Cardiac function Autophagy of cardiac myocytes |
| 基金项目:北京市2017年保健科研（调研）课题（京17-12） |
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| 中文摘要: |
| 摘要 目的：研究曲美他嗪对心肌梗死后心力衰竭大鼠炎症反应、氧化应激及心肌细胞自噬的影响。方法：将51只SD大鼠纳入研究，遵循随机数字表法分成假手术组、模型组及干预组，每组17只。模型组与干预组大鼠均以结扎冠状动脉前降支近段法完成心肌梗死后心力衰竭大鼠模型的制备，假手术组仅开腹暴露，分离双侧肾动脉间腹主动脉，但不实施缩窄处理，其余步骤和模型组以及干预组一致。造模成功后，模型组与假手术组大鼠分别予以生理盐水灌胃处理，干预组大鼠则予以曲美他嗪灌胃处理。比较各组大鼠心功能，炎症反应，氧化应激以及心肌细胞自噬情况。结果：模型组、干预组左心射血分数（LVEF）均低于假手术组，但干预组高于模型组；模型组、干预组的左心室收缩末期内径（LVESD）、左心室舒张末期内径（LVEDD）均高于假手术组，但干预组低于模型组（均P＜0.05）。模型组、干预组的C反应蛋白（CRP）、肿瘤坏死因子-α（TNF-α）及白细胞介素-6（IL-6）水平均高于假手术组，但干预组低于模型组（均P＜0.05）。模型组、干预组的丙二醛（MDA）水平均高于假手术组，但干预组低于模型组；模型组、干预组的超氧化物歧化酶（SOD）水平均低于假手术组，但干预组高于模型组（均P＜0.05）。模型组、干预组的LC3-Ⅱ、Beclin-1蛋白相对表达量均高于假手术组，且干预组高于模型组（均P＜0.05）。结论：曲美他嗪可有效改善心肌梗死后心力衰竭大鼠心功能，同时减轻炎症反应与氧化应激反应，有效促进心肌细胞自噬因子表达。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effects of trimetazidine on the inflammatory response, oxidative stress and autophagy of cardiac myocytes in rats with heart failure after myocardial infarction. Methods: 51 SD rats were included in the study, and were randomly divided into sham operation group, model group and intervention group according to the random number table method, with 17 rats in each group. The rat model of heart failure after myocardial infarction was prepared by ligating the proximal segment of the anterior descending coronary artery in both the model group and the intervention group. The sham operation group was exposed only by laparotomy to separate the abdominal aorta between bilateral renal arteries without constriction, which was consistent with the procedure and the model group as well as the intervention group. After successful modeling, rats in the model group and the sham operation group were given normal saline gavage, and rats in the intervention group were given trimetazidine gavage. Cardiac function, inflammatory response, oxidative stress and autophagy of cardiac myocytes were compared in each group. Results: Left ventricular ejection fraction (LVEF) in the model group and the intervention group were lower than that in the sham operation group, and the intervention group was higher than that in the model group. Left ventricular end systolic diameter (LVESD), left ventricular end diastolic diameter (LVEDD) in the model group and the intervention group were higher than those in the sham operation group, and the intervention group was lower than that in the model group (all P<0.05). The C-reactive protein (CRP), tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) levels of the model group and the intervention group were higher than those of the sham operation group, and the intervention group was lower than that of the model group (all P<0.05). The malondialdehyde (MDA) level of the model group and the intervention group were higher than that of the sham operation group, and the intervention group was lower than that of the model group. The level of superoxide dismutase (SOD) in the model group and the intervention group was lower than that in the sham operation group, and the intervention group was higher than that in the model group (all P<0.05), Model group and intervention group of LC3 - Ⅱ, Beclin 1 protein expression of relative quantity were higher than in sham operation group, and the intervention group was higher than model group (all P<0.05). Conclusion: Trimetazidine can effectively improve cardiac function in heart failure rats after myocardial infarction, reduce inflammatory response and oxidative stress response, and effectively promote the expression of autophagy of cardiac myocytes. |
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