Cardiology Department, Tianjin Huaxing Hospital, Tianjin 300270, China.
Cadre's Ward, Characteristic Medical Center of Chinese People's Armed Police Force 300, Tianjin 300171, China.
Biomed Res Int. 2021 Jul 9;2021:9931885. doi: 10.1155/2021/9931885. eCollection 2021.
To investigate the role and mechanism of aspirin in myocardial injury induced by myocardial ischemia-reperfusion in rats through STAT3 signaling pathway.
Sixty rats were randomly divided into three groups: the sham operation group, MI/R group, and MI/R+aspirin group (aspirin group). The rats in the sham operation group did not ligate the LAD coronary artery, while the aspirin group ligated the LAD coronary artery, which caused the suture to be loosened after 30 minutes ischemia, and 60 mg/kg aspirin was injected into the tail vein 10 minutes before reperfusion. After three hours of reperfusion, the ultrasound system was used to collect hemodynamic parameters, including ejection fraction (EF%), shortening fraction (FS%), and left ventricular end-systolic pressure (LVESP%) and left ventricular end-diastolic pressure (LVEDP%). Finally, the rats were euthanized; then, blood samples were taken for biochemical examination, myocardial tissue was collected, and the left ventricle was used for subsequent experiments. The gene expression levels of Bax and Bcl-2 were detected by PCR. The protein expression levels of Bcl-2, Bax, p-JAK2, total JAK2, p-STAT3, and total STAT3 were detected by Western blot.
Compared with the sham operation group and the aspirin group, the area of myocardial infarction in the MI/R was significantly increased ( < 0.05). In terms of hemodynamic parameters, LVEDP was significantly elevated in the MI/R group. The results of PCR showed that compared with the MI/R group, the mRNA expression of Bax in the aspirin group was significantly decreased, while that of Bcl-2 was significantly increased ( < 0.05). Western blot analysis showed that compared with the MI/R group, aspirin pretreatment significantly increased the expression levels of p-STAT3 and p-JAK2 ( < 0.05).
The mechanism of aspirin preconditioning to protect the heart from MI/R injury appears to be related to JAK2/STAT3 and related to the activation of the signaling pathway.
通过 STAT3 信号通路探讨阿司匹林在大鼠心肌缺血再灌注损伤致心肌损伤中的作用及机制。
60 只大鼠随机分为 3 组：假手术组、MI/R 组和 MI/R+阿司匹林组（阿司匹林组）。假手术组不结扎 LAD 冠状动脉，阿司匹林组结扎 LAD 冠状动脉，缺血 30min 后松开缝线，再灌注前 10min 尾静脉注射 60mg/kg 阿司匹林。再灌注 3h 后，应用超声系统采集射血分数（EF%）、缩短分数（FS%）、左心室收缩末期压（LVESP%）和左心室舒张末期压（LVEDP）等血流动力学参数。处死大鼠后采血行生化检查，取心肌组织，左心室用于后续实验。PCR 检测 Bax 和 Bcl-2 的基因表达水平。Western blot 检测 Bcl-2、Bax、p-JAK2、总 JAK2、p-STAT3 和总 STAT3 的蛋白表达水平。
与假手术组和阿司匹林组比较，MI/R 组心肌梗死面积明显增大（ < 0.05）。血流动力学参数方面，MI/R 组 LVEDP 明显升高。PCR 结果显示，与 MI/R 组比较，阿司匹林组 Bax mRNA 表达明显降低，Bcl-2 表达明显升高（ < 0.05）。Western blot 分析显示，与 MI/R 组比较，阿司匹林预处理明显增加 p-STAT3 和 p-JAK2 的表达水平（ < 0.05）。
阿司匹林预处理对心肌缺血再灌注损伤的心脏保护作用机制可能与 JAK2/STAT3 及相关信号通路激活有关。
