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Fig. 2 | Biology Direct

Fig. 2

From: Circulating extracellular vesicles regulate ELAVL1 by delivering miR-133a-3p which affecting NLRP3 mRNA stability inhibiting PANoptosome formation

Fig. 2

Effects of EVs from different sources on cardiac function in a mouse model of acute myocardial infarction. (A) Schematic diagram of the in vivo experimental design. Legend: Schematic diagram of the in vivo experimental design. The timeline shows the key steps and time points for the myocardial infarction (MI) model, including surgery, treatment administration, and endpoint measurements. Mice were randomly divided into the control group and the treatment group. The treatment group received N-EVs (50 µg/mL) intravenously, while the control group received an equal volume of PBS. Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured at 2 weeks and 4 weeks post-MI using echocardiography. The figure illustrates the overall experimental setup and timeline. (B-C) The left ventricular ejection fraction (LVEF) was assessed using echocardiography at baseline (1 day prior to myocardial infarction) and endpoint (3 weeks after myocardial infarction). Legend: Echocardiographic assessment of left ventricular ejection fraction (LVEF) was performed at baseline (1 day before myocardial infarction) and at the endpoint (3 weeks after myocardial infarction). The LVEF values at both time points are presented as mean ± standard deviation (SD). (D) Myocardial tissue staining confirmed the therapeutic effects of N-EVs and AMI-EVs on hypoxia/reoxygenation injury. Legend: Myocardial tissue sections were stained with HE, Masson’s trichrome and TUNEL to assess collagen deposition and fibrosis. The figure shows representative images of myocardial tissue from the control group (PBS), N-EVs treatment group, and AMI-EVs treatment group. The extent of fibrosis is quantified as the ratio of fibrotic area to total ventricular area. The therapeutic effects of N-EVs and AMI-EVs on reducing hypoxia/reoxygenation injury are evident from the reduced fibrosis in the treatment groups compared to the control group. Scale bar: 100 μm. (E-F) QRT-PCR and WB were employed to investigate the impact of circulating EVs from different sources on the expression of angiogenic markers. Legend: (E) Quantitative real-time PCR (QRT-PCR) was used to measure the mRNA expression levels of angiogenic markers (VEGF, Ang-1, and HIF-1α) in myocardial tissue. (F) Western blot (WB) analysis was performed to evaluate the protein expression levels of the same angiogenic markers. The figure shows the relative expression levels of these markers in the control group (PBS), N-EVs treatment group, and AMI-EVs treatment group. Statistical analysis revealed a significant difference (*P < 0.05) compared to the PBS group, as well as a significant difference (#P < 0.05) compared to the AMI-EVs group

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