Fig. 6
AAV9-S100a9-RNAi improved β1-AA-induced cardiac dysfunction and decrease in myocardial autophagic flux in mice. A Fluorescence detection of virus enrichment in frozen sections of myocardium. B Western blot analysis was used to determine the level of S100a9 in the myocardial tissue of the AAV9-Vector-RNAi group and AAV9-S100a9-RNAi group. C M-mode echocardiography images of immunized mice. D A small animal ultrasound was used to detect the EF%, FS%, LVIDd, LVIDs, IVSd, and IVSs (n = 8 per group). E Western blot analysis was used to determine the levels of S100a9, HIF-1α, Atg9a, LC3, and p62 (n = 6 per group). F Statistical chart of the expression levels of S100a9, HIF-1α, Atg9a, LC3, and p62 in the myocardial tissue. Data are presented as the mean ± SEM; *p < 0.05 vs. control, **p < 0.01 vs. control, and #p < 0.05 vs. β1-AA group, ##p < 0.01 vs. β1-AA group