Ischemia/reperfusion (I/R) injury causes complications in early coronary artery reperfusion for acute myocardial infarction (AMI). Ozone (O 3 ) has been reported to be applied for protecting I/ R injury, but its detailed mechanism remains unclear. Our study focused on the protective effect of O 3 pretreatment on myocardial I/R injury and JAK2/STAT3 signaling and HSP70 regulation involving in the mediation. The rat hearts which were perfused and isolated as well as the cultured cardiomyocytes of neonatal rat were exposed to hypoxia/reoxygenation (H/R) and different concentrations of O 3 followed by heat shock protein 70 (HSP70) siRNA treatment. The results showed O 3 attenuated the suppression of cell viability induced by H/R and decreased the release of activity of creatine kinase (CK), lactate dehydrogenase (LDH) and apoptosis of cardiomyocytes in vitro. Moreover, O 3 also activated the JAK2/STAT3 signaling, upregulated the expression of HSP70 both in vitro and vivo, and decreased the index of apoptosis of cardiomyocytes caused by I/ R as well as myocardial infarct area in vivo. In addition, HSP70 siRNA and JAK2 inhibitor AG490 inhibited the cardioprotective effect of O 3 . And the expression of HSP70 increased by ozone was reduced by AG-490. In conclusion, our results demonstrated that ozone protects cardiomyocytes in I/R injury through regulation of the expression of HSP70 by activating the JAK2/STAT3 pathway.

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BackgroundTo evaluate the advantages and disadvantages of anticoagulant therapy and provide a piece of information on anti-thrombotic treatment strategies for patients with new-onset atrial fibrillation (NOAF) and acute myocardial infarction (AMI).MethodsLiterature from PubMed and Google scholar were screened until August 2022. Studies assessing oral anticoagulant (OAC) treatments for NOAF in patients with AMI were evaluated for inclusion.ResultsThree retrospective cohort studies were included. In the study performed by Madsen et al., patients with previously diagnosed AMI with or without NOAF were followed up for 5.8 years. About 38% of NOAF patients with anticoagulant therapies, which could reduce long-term mortality [adjusted hazard ratio (HR): 0.69; 95% confidence interval (CI): 0.47–1.00]. Hofer et al. performed a single-center cohort study containing 1,372 patients with AMI with an 8.6-year follow-up period. Dual anti-thrombotic therapy (DAT) did not show the effect on the survival in NOAF (adjusted HR: 0.97; 95% CI: 0.65–1.57), while triple antithrombotic therapy (TAT) could reduce long-term cardiovascular mortality (adjusted HR: 0.86; 95% CI: 0.45–0.92). Petersen et al. also did a cohort study with 1-year follow-up duration. It showed that anticoagulant therapies demonstrated positive results (HR: 0.78; 95% CI: 0.41–1.47).ConclusionRecent studies have shown that anticoagulant therapy in AMI-NOAF patients can obviously reduce the mortality of AMI-NOAF patients, especially OAC therapy. Further clinical trials could confirm these findings.