Cx43蛋白介导的磷酸肌酸对心肌缺血/再灌注损伤的保护作用。

IF 1.8 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Cardiology Research and Practice Pub Date : 2021-01-22 eCollection Date: 2021-01-01 DOI:10.1155/2021/8838151
Chen-Xi Wang, Jun-Jun Guo, An-Jie Di, Yu Zhu, Wei-Min Han, An-Ran Cheng, Cheng Li, Rui-Chan Si, Tian-Shu Lan, Ran Zhang, Hong-Li Liu, Guo-Liang Yan
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引用次数: 3

摘要

目的:验证磷酸肌酸对心肌缺血模型的保护作用及其可能的作用机制。方法:采用结扎球囊法建立大鼠心肌缺血再灌注模型。30只SD大鼠随机分为3组,每组10只。假手术组:未阻断冠状动脉,观察120分钟。缺血再灌注(I/R)组缺血30 min,缺血再灌注90 min。磷酸肌酸(PCr)组:缺血30分钟后,腹腔注射PCr (200 mg/kg) 90分钟。体外心肌缺血再灌注模型动物组与体内组相同。开胸取心,立即用H-K缓冲液冲洗。然后,心脏被安装在Langendorff仪器上。PCr组灌注液浓度为10 mmol/L。记录离体心肌冠状动脉血流变化。用RM6240BT记录仪记录心率和心电图。实验结束时,做心肌病理切片和Cx43免疫荧光染色,检测心肌组织丙二醛(MDA)含量。结果:磷酸肌酐治疗改善了心肌缺血模型,改善了心电图(ECG)改变(ST段明显)和组织学改变(坏死心肌细胞减少,炎症细胞浸润减少,心肌水肿减轻)。同时,MDA降低,冠状动脉血流量和Cx43表达明显改善。结论:磷酸肌酸能改善心电图,恢复缺血心肌和冠状动脉血流的组织学改变。其机制可能是通过抑制自由基的产生和恢复Cx43蛋白的表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury.

The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury.

The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury.

The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury.

Objectives: To verify the protective effect of phosphocreatine on myocardium in an ischemic model and the possible mechanism of action.

Methods: The model of myocardial ischemia/reperfusion (I/R) was established by the ligation balloon method. 30 SD rats were randomly divided into three groups, n = 10 in each group. Sham operation group: the coronary artery was not blocked and observed for 120 minutes. The ischemia/reperfusion (I/R) group was given ischemia for 30 minutes and ischemia reperfusion for 90 minutes. Phosphocreatine (PCr) group: after 30 minutes of ischemia, the rats were intraperitoneally injected with PCr (200 mg/kg) for 90 minutes. The animal groups of myocardial ischemia/reperfusion model in vitro were the same as those in vivo. The heart was removed by thoracotomy and washed immediately in H-K buffer solution. Then, the heart was installed on the Langendorff instrument. The concentration of PCr perfusion fluid in the PCr group was 10 mmol/L. The changes in coronary blood flow in isolated myocardium were recorded. The heart rate and electrocardiogram were recorded by RM6240BT. At the end of the experiment, myocardial pathological sections and Cx43 immunofluorescence staining were made, and the contents of malondialdehyde (MDA) in myocardial tissue were detected.

Results: Phosphocreatinine treatment improved the myocardial ischemia model, performance in electrocardiogram (ECG) changes (ST segment apparent), and histological changes (decrease in necrotic myocardial cells, inflammatory cell infiltration, and a reduction in myocardial edema). At the same time, MDA decreased, while coronary blood flow and Cx43 expression significantly improved.

Conclusions: Phosphocreatine can improve the electrocardiogram and restore histologic changes in ischemic myocardium and coronary blood flow. The postulated mechanism is by inhibiting the generation of free oxygen radicals and restoring the expression of Cx43 protein.

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来源期刊
Cardiology Research and Practice
Cardiology Research and Practice Medicine-Cardiology and Cardiovascular Medicine
CiteScore
4.40
自引率
0.00%
发文量
64
审稿时长
13 weeks
期刊介绍: Cardiology Research and Practice is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies that focus on the diagnosis and treatment of cardiovascular disease. The journal welcomes submissions related to systemic hypertension, arrhythmia, congestive heart failure, valvular heart disease, vascular disease, congenital heart disease, and cardiomyopathy.
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