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. 2021 Jul 25;11(17):8550–8569. doi: 10.7150/thno.61875

Figure 5.

Figure 5

Therapeutic effects of inhaled TPCD NP on DOX-induced heart failure in mice. (A) Schematic illustration of the treatment protocols. (B) Typical digital photos show hearts isolated from mice in different groups. (C) The heart weight of different groups. (D) Ratios of HW/TL for different groups. (E) Representative M-mode echocardiography images of mouse hearts after different treatments. (F-G) Left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) quantified by echocardiography. (H-I) The levels of MDA (H) and H2O2 (I) in tissue homogenates of hearts from mice treated with different formulations. The total protein content in heart homogenates was measured by the BCA assay. (J-K) Fluorescence images (J) and quantitative analysis (K) of DHE-stained heart cryosections for mice subjected to different treatments. (L-M) Serum levels of cTnI (L) and CK-MB (M). (N) H&E-stained histological sections of hearts. Control, healthy mice treated with saline; DOX, mice treated with DOX and saline. In different TPCD NP groups, diseased mice were treated with different doses of TPCD NP. Scale bars: 3 mm (B), 500 μm (J), 20 μm (N). Data in (C-D,F-I,K-M) are mean ± SD (n = 5). Statistical significance was assessed by the one-way ANOVA with post-hoc LSD tests. *P < 0.05, **P < 0.01, ***P < 0.001.