Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway

Figure 2

ApoE deficiency promotes neutrophil activation. (a, b) Representative immunofluorescent staining of Ly6G within infarcted hearts of WT and ApoE^-/- mice 1 day after ligation and the percentage of the Ly6G-positive area of the whole image. Scale bars: 100 μm. Each group involves 6 mice. (c, d) The gating strategy of flow cytometry and the percentage of myeloid cells (CD11b⁺) and neutrophils (CD11b⁺ Ly6G^high Ly6C^low) in the blood of ApoE^-/- and WT mice 1 day after infarction. Each group involves 8 mice. (e) Quantitative real-time PCR of proinflammation cytokines of tumor necrosis factor (Tnf), interleukin 1 beta (Il1b), and interleukin 6 (Il6) in infarcted hearts of ApoE^-/- and WT mice without surgery (Ctrl) and 1 day after infarction (MI). Each group involves 6 mice. (f, g) Quantitative real-time PCR of integrin alpha-M (Itgam), neutrophil myeloperoxidase (Mpo), and neutrophil elastase (Elane) in infarcted hearts of ApoE^-/- and WT mice without surgery (Ctrl) and 1 day after infarction (MI). Each group involves 6 mice. Data are shown as . Statistical tests include the two-tailed Student’s -test (two groups) and one-way analysis of variance followed by Tukey’s multiple comparison test (more than two groups). and .

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