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Fig. 2 | BMC Medicine

Fig. 2

From: Atorvastatin-pretreated mesenchymal stem cell-derived extracellular vesicles promote cardiac repair after myocardial infarction via shifting macrophage polarization by targeting microRNA-139-3p/Stat1 pathway

Fig. 2

The superior effects of MSCATV-EV on ventricular function, MI size, macrophage infiltration and M2 polarization in AMI rats. A Representative M-mode echocardiogram of each group on day 28 after AMI. B The dynamic changes in LVEF, LVFS, LVESV, and LVEDV of each group on days 0, 3, 7, 28 after AMI, n = 6–7 per group. C Representatives of heart cross sections with Masson trichrome staining on day 28. D Quantification of infarct size of each group in C, n = 6–7 per group. E Representative confocal images of CD68+ or CD206+ macrophages within the infarct border zone on day 3 post-AMI. F Quantification of CD68+ or CD206+ macrophages in E, n = 6-7 per group. G Western blot analysis of iNOS and Arg1 expressions in infarcted myocardium of each group. H Quantification of iNOS and Arg1 expressions in G, n = 3 per group. I The mRNA expressions of M1 (iNOS, IL-12, TNF-α) and M2 (Arg1, IL-10, CD206) macrophage markers in infarcted zone measured by qPCR, n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Arg1, arginase 1; AMI, acute myocardial infarction; ATV, atorvastatin; EV, extracellular vesicle; IL, interleukin; iNOS, inducible nitric oxide synthase; LVEDV, left ventricular end diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; LVFS, left ventricular fractional shortening; MSCs, mesenchymal stem cells; qPCR, quantitative polymerase chain reaction; TNF-α, tumor necrosis factor alpha

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