Fig. 3

(HR + P)-EMVs showed less effects on inducing cardiac injury compared with HR-EMVs in ischemia-reperfused hearts. (A) Protocol schematic for infusion of EMVs and tissue harvest. (B) Bioluminescence imaging showing uptake of PKH26-labelled EMVs by cardiomyocytes. Mice were randomly divided into 6 groups: sham/IR + PBS, sham/IR + HR-EMVs, sham/IR+(HR + P)-EMVs, 5 mice per group, and 50 ul EMVs (10^9 particles/ml) were injected intracardially: (C) Plasma lactate dehydrogenase (LDH) activity in mice. (D) Echocardiographic assessment of cardiac function. (E) Quantitative analysis of left ventricular ejection fraction (LVEF). (F) Quantitative analysis of left ventricular shortening fraction (LVFS). Mice were randomly divided into 4 groups: sham + PBS, IR + PBS, IR + HR-EMVs, IR + (HR + P)-EMVs, 5 mice per group,and 50 ul EMVs (10^9 particles/ml) were injected intracardially: (G) Evans blue-TTC staining for detection of myocardial infarct area. Area-at-risk (AAR; black line), infarct size (white dotted line), scale bar = 5 mm. (H) Quantitative analysis of the percentage AAR and percentage infarct of hearts in (G). (I) Myocardial tissue ROS levels were detected by fluorescence microscopy after DHE staining of heart sections. (J) Quantitative analysis of DHE staining. (K) Fluorescence microscopy of cardiac sections after TUNEL staining to detect apoptosis levels in cardiac myocytes. (L) Quantification of TUNEL staining. (M-N) Western blotting analysis was performed for Bax, Bcl-2, and cleaved caspase-3 in heart tissue, and relative grayscale was calculated by ImageJ software. These data were representative results (n = 5) of five repetitions. *P < 0.05, **P < 0.01, ***P < 0.001, ns, not significant. Data are expressed as mean ± SEM.