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
The Protective Effect of Cx43 Protein-Mediated Phosphocreatine on Myocardial Ischemia/Reperfusion Injury.
作者信息
Wang Chen-Xi, Guo Jun-Jun, Di An-Jie, Zhu Yu, Han Wei-Min, Cheng An-Ran, Li Cheng, Si Rui-Chan, Lan Tian-Shu, Zhang Ran, Liu Hong-Li, Yan Guo-Liang
机构信息
School of Medicine, Xiamen University, Xiamen 361100, China.
Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Xiamen 361100, China.
出版信息
Cardiol Res Pract. 2021 Jan 22;2021:8838151. doi: 10.1155/2021/8838151. eCollection 2021.
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, = 10 in each group. Sham operation group: the coronary artery was not blocked and observed for 120 minutes. The ischemia/reperfusion (/) 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.
目的
验证磷酸肌酸在缺血模型中对心肌的保护作用及其可能的作用机制。
方法
采用结扎气囊法建立心肌缺血/再灌注（I/R）模型。将30只SD大鼠随机分为三组，每组10只。假手术组：不阻断冠状动脉，观察120分钟。缺血/再灌注（I/R）组：缺血30分钟，再灌注90分钟。磷酸肌酸（PCr）组：缺血30分钟后，大鼠腹腔注射PCr（200mg/kg），持续90分钟。体外心肌缺血/再灌注模型的动物分组与体内相同。开胸取出心脏，立即置于H-K缓冲液中冲洗。然后，将心脏安装在Langendorff仪器上。PCr组PCr灌注液浓度为10mmol/L。记录离体心肌冠状动脉血流量的变化。用RM6240BT记录心率和心电图。实验结束时，制作心肌病理切片和Cx43免疫荧光染色，检测心肌组织中丙二醛（MDA）含量。
结果
磷酸肌酸治疗改善了心肌缺血模型，心电图（ECG）变化（ST段明显）和组织学变化（坏死心肌细胞减少、炎症细胞浸润和心肌水肿减轻）表现良好。同时，MDA降低，而冠状动脉血流量和Cx43表达显著改善。
结论
磷酸肌酸可改善缺血心肌的心电图，恢复组织学变化和冠状动脉血流量。推测其机制是通过抑制氧自由基的产生和恢复Cx43蛋白的表达。
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