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Fig. 2 | BMC Pharmacology and Toxicology

Fig. 2

From: Premedication with pioglitazone prevents doxorubicin-induced left ventricular dysfunction in mice

Fig. 2

Pio improved vacuolization but showed no significant biochemical or physiological changes in the acute phase of DOX-induced LV dysfunction mice (day 7). a Representative images of hematoxylin-eosin (HE) staining of a heart from each group. Scale bar, 50 μm. b Summary data of the cross-sectional area (CSA) of the left ventricle on HE staining. n = 3 for each group. c Number of vacuolization in cells in the HE stained samples of each sample, calculated as the percentage of cells containing vacuoles, i.e., 0: none; 1: less than 25%; 2: 25–50%; and 3: more than 50%. d Representative images of Masson trichrome (MT) staining of a heart from each group. Scale bar, 50 μm. e Summary data of fibrosis area in the MT-stained samples. n = 3 for each group. f, g Quantitative analysis of the gene expression levels of interleukin-1beta (Il1b) and tumor necrosis factor-alpha (Tnfa) in the heart on day 7 (n = 7–10 for each group). h Hydrogen peroxide (H2O2) release originating from non-fatty-acid substrates from isolated mitochondria in hearts during state 3 respiration (i.e. oxidative phosphorylation) using the complex I- and II-linked substrates glutamate, malate, and succinate (n = 3 for each group). i Levels of mitochondrial iron contents (n = 4–8 for each group). j Mitochondrial respiration using non-fatty-acid substrates in isolated mitochondria from the heart during state 3 respiration using the complex I- and II-linked substrates glutamate, malate, and succinate (n = 3 for each group). k Mitochondrial respiration with fatty-acid substrate (octanoyl-l-carnitine) in isolated mitochondria from the heart during state 3 respiration (n = 3 for each group). Data are shown as means ± SEs. *P < 0.05 vs. Vehicle. NS, not significant

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