Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis.

Introduction: Naringenin exerts a protective effect on myocardial ischemia and reperfusion. It has been reported that miR-223-3p is a potential target for the treatment of myocardial infarction (MI). In view of the unreported correlation between Naringenin and miR-223-3p, this study was designed to confirm that the ameliorative effects of Naringenin on MI is directly related to the regulation of miR-223-3p. Methods: Through electrocardiogram detection, Masson pathological staining and immunohistochemistry of angiogenesis-related factors, alleviative effects of Naringenin on heart function, myocardial injury and angiogenesis in MI mice were observed individually. Hypoxic HUVECs were selected in the in vitro experimental model. The cell viability, angiogenesis and migration ability were analyzed to fathom out the pro-angiogenesis potential of Naringenin. The effect of Naringenin on miR-223-3p, as well as the downstream molecular mechanism was verified through bioinformatics analysis and rescue experiments. Results: Naringenin improved heart functions of MI mice, reduced degree of myocardial fibrosis, stimulated expressions of angiogenic factors and down-regulated level of miR-223-3p in myocardial tissue. In in vitro experiments, Naringenin increased the viability of hypoxic HUVECs, as well as the abilities of tube formation and migration, and further inhibited the expression of miR-223-3p. In the rescue trial, miR-223-3p mimic reversed the therapeutic effect of Naringenin. Type 1 insulin-like growth factor receptor (IGF1R), as a downstream target gene of miR-223-3p, partially offset the cellular regulatory effects of miR-223-3p after overexpression of IGF1R. Conclusions: Naringenin improves the angiogenesis of hypoxic HUVECs by regulating the miR-223-3p/IGF1R axis, and has the potential to promote myocardial angiogenesis in MI mice.

Prognostic value of the SYNTAX score on myocardial injury and salvage in STEMI patients after primary percutaneous coronary intervention: a single-center retrospective observational study.

BACKGROUND: SYNTAX score (SS) was shown to positively correlate with postprocedural myocardial injury in patients after elective coronary artery intervention, but evidence about the association of SS with myocardial salvage in ST-segment elevation myocardial infarction (STEMI) patients is still needed. This study aimed to evaluate the prognostic value of SS for myocardial injury and salvage assessed by cardiac magnetic resonance (CMR) after primary percutaneous coronary intervention (PCI) in STEMI patients. METHODS: This single-center retrospective study consecutively enrolled STEMI patients who had undergone primary PCI within 12 h from symptom onset. Both angiography and CMR were performed during hospitalization, and patients were divided into low SS (SS ≤ 22), mediate-high SS (SS > 22) groups. Correlation and multivariable analyses were performed. RESULTS: A total of 149 STEMI patients (96 low SS, 53 mediate-high SS) were included. In terms of myocardial injury parameters, there was a positive correlation (p < 0.001, Spearman r = 0.292) between SS and infarct size (IS), and a negative correlation (p < 0.001, Spearman r = - 0.314) between SS and myocardial salvage index (MSI). In the multivariable model, SS (> 22 as categorical variable, OR = 2.245, 95% CI [1.002-5.053], p = 0.048; as continuous variable, OR = 1.053, 95% CI [1.014-1.095], p = 0.008) was significantly associated with high IS (≥ mean 35.43). The areas under the receiver operating characteristic (ROC) curves of SS for high IS and low MSI (≤ median 28.01) were 0.664 and 0.610. CONCLUSIONS: In STEMI patients undergoing primary PCI, SYNTAX score positively correlated with infarct size and negatively with myocardial salvage, indicating an independent predictive value of the myocardial injury.

Different Changing Patterns of Three NOS-NO System Activities after Ischemia-Reperfusion in Rabbit with AMI.

NOS-NO system activity is closely correlated with ischemia-reperfusion injury (IRI) and NOS subtypes were suggested to play different roles in IRI. In this work, the activity of serum NOS, NO levels, and ischemic necrosis after reperfusion in rabbit with AMI at different time was studied. We also explored the NOS-NO system activity changes and its correlation with myocardial ischemia and necrosis. It shows that after reperfusion in rabbits with AMI, NO-NOS system activities present different changes at each time point due to inactivation of NO and iNOS activation, and different experimental animals, ischemia-reperfusion degree, and length of time will also lead to different research results. Therefore, it is necessary to conduct dynamic observation on animals from different species at multi-temporal point under the state of NOS-NO system activities, and simultaneously detect inflammatory factor, MDA, and SOD indexes. Therefore, it is a must to conduct relevant drug research studies to make NOS-NO system activities maintain the level in favor of ideal myocardial ischemia reperfusion.