Research Paper Volume 13, Issue 16 pp 20569—20584

NPAS2 ameliorates myocardial ischaemia/reperfusion injury in rats via CX3CL1 pathways and regulating autophagy

NPAS2 was downregulated in myocardial ischaemia/reperfusion injury rats. (A, B) Typical images of H&E and Masson staining of myocardial tissue segments. (C, D) Typical images of TTC of myocardial tissue segments. The infarct size was measured and calculated as a percentage of the total area. (E, F) Typical images of Tunel of myocardial tissue segments. The relative percentages of apoptotic cells were calculated. (G, H) Typical echocardiographic images of M-mode and LVEF. (I) The mRNA level of NPAS2 in rat myocardial tissue was determined by qRT-PCR. (J) The protein level of NPAS2 (90kDa), LC3B (14 and 16kDa) and p62 (62kDa) in rat myocardial tissue was determined using Western Blot. Data are expressed as mean ± SEM (n = 6).

Figure 1. NPAS2 was downregulated in myocardial ischaemia/reperfusion injury rats. (A, B) Typical images of H&E and Masson staining of myocardial tissue segments. (C, D) Typical images of TTC of myocardial tissue segments. The infarct size was measured and calculated as a percentage of the total area. (E, F) Typical images of Tunel of myocardial tissue segments. The relative percentages of apoptotic cells were calculated. (G, H) Typical echocardiographic images of M-mode and LVEF. (I) The mRNA level of NPAS2 in rat myocardial tissue was determined by qRT-PCR. (J) The protein level of NPAS2 (90kDa), LC3B (14 and 16kDa) and p62 (62kDa) in rat myocardial tissue was determined using Western Blot. Data are expressed as mean ± SEM (n = 6).