Abstract
Objective To investigate the role and mechanism of aspirin in myocardial injury induced by myocardial ischemia-reperfusion in rats through STAT3 signaling pathway. Methods 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. Results Compared with the sham operation group and the aspirin group, the area of myocardial infarction in the MI/R was significantly increased (p < 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 (p < 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 (p < 0.05). Conclusion 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.
Highlights
Ischemic heart disease (IHD), the most common cardiovascular disease in human, is one of the leading causes of death in the world [1].) The most effective method to reduce the infarct size and maintain cardiac function after acute myocardial infarction is myocardial reperfusion [2] that requires blood reperfusion of ischemic myocardium to restore the oxygen supply to the myocardium and improve the biological function of ischemic myocardium
The myocardial infarction size was greater in the myocardial ischemia-reperfusion (MI/R) group and MI/R+aspirin group than that in the sham operation group, confirmed by TTC staining results (p < 0:01), and it was significantly reduced after treatment with aspirin (p < 0:01) (Figure 2)
PCR and Western Blot Test Results. Compared with those in the sham operation group, the messenger ribonucleic acid (mRNA) expression of Bcl-2-associated X protein (Bax) was clearly raised, while that of B-cell lymphoma 2 (Bcl-2) was distinctly lowered in the MI/R group (p < 0:05)
Summary
Ischemic heart disease (IHD), the most common cardiovascular disease in human, is one of the leading causes of death in the world [1].) The most effective method to reduce the infarct size and maintain cardiac function after acute myocardial infarction is myocardial reperfusion [2] that requires blood reperfusion of ischemic myocardium to restore the oxygen supply to the myocardium and improve the biological function of ischemic myocardium. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signal transduction pathway is an important cellular signal transduction pathway transducing signals from the plasma membrane to nuclear cells and playing a key role in regulating cardiac protection against I/R injury [5, 6]. The JAK2/STAT3 signaling pathway has been proven to be able to prevent I/R injury [7]. In. BioMed Research International addition, the JAK/STAT signaling pathway participates in the growth, development, proliferation, apoptosis, and necrosis of cells [8]. The JAK/STAT signal transduction pathway activates many cytokines under the control of the following drugs after MI/R injury. Phosphorylation-activated JAK2 and STAT3 mediate the apoptosis of myocardial cells, which is regarded as an important pathological mechanism of apoptosis after MI/R injury [9, 10]
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