Quercetin prevents myocardial infarction adverse remodeling in rats by attenuating TGF-β1/Smad3 signaling: Different mechanisms of action

Figures

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  Fig. 1. Average heart weights (A) and serum levels of creatinine kinase-MB (B), angiotensin II (ANG II) (C), and Troponin- 1 (D) in all groups of rats. Data are expressed as mean ± SD of 12 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.

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  Fig. 2. Cardiac hemodynamic function in the hearts of all groups of rats. Data are expressed as mean ± SD of 12 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats. LVEDP: LV end-diastolic pressure. LVSP: LV systolic pressure.

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  Fig. 3. Photomicrographs of the non-infracted left ventricles (LVs) of all groups of rats. (200X). A and B: were taken from corresponding areas of the LVs of the control (sham-operated) and control + Quercetin (QUR)-treated rats and showed intact muscle fibers (red arrow), intercalated disk (arrowhead), cardiomyocytes nuclei (long black arrow) and endothelial nuclei (short black arrow). C & D: were taken from the remote myocardia of the LVs of myocardial infarcted (MI)-induced rats and showed abnormalities in the organization of myofibrils, hypertrophied muscle fibers (long black arrow), damaged muscle fibers (red arrow), infiltration of inflammatory cells (yellow arrow), and nuclear fading (Karyolysis) (short black arrow). E and F: were taken from the remote myocardia of the LVs of MI+ treated rats and showed much improvement in the structure and orientation of the myofibrils (long black arrow), as well as a normal size of the myofibrils (red arrow). Also, the endothelial and cardiomyocytes nuclei appeared normal (short black arrow). However, few infiltrating cells were still observed (yellow arrow) with no obvious cardiomyocytes damage.

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  Fig. 4. Levels of tumor necrosis factor (TNF-α) (A), interleukin-6 (IL-6) (C), and angiotensin II (ANG II) (C), as well as the nuclear activity (D) and levels (E) of NF-kB in the viable non-infarcted myocardia of the left ventricles (LVs) of all groups of rats. Data are expressed as mean ± SD of 6 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.

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  Fig. 5. Levels of reactive oxygen species (ROS), malondialdehyde (MDA) (B), superoxide dismutase (SOD) (C), and reduced glutathione (GSH) (D), as well protein levels of the nuclear factor erythroid 2–related factor 2 (Nrf-2) (E) in the viable non-infarcted myocardia of the left ventricles (LVs) of all groups of rats. Data are expressed as mean ± SD of 6 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.

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  Fig. 6. Photomicrographs of the left ventricles (LVs) of rats from all experimental groups as stained by Masson’s trichrome stain (A-F) and protein levels of collagen 1A1 and 3A1 (G) in the viable non-infarcted myocardia of the LVs of all groups of rats. Collagen deposition is indicated by the blue color. A and B: were taken from the corresponding LVs sham-operated (control) and control + QUR-treated rats. C and D: were taken from the remote myocardia myocardial infarcted (MI) hearts. E and F: were taken from the remote myocardia of MI + QUR-treated rats. In G: data are expressed as mean ± SD of 6 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.

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  Fig. 7. Protein levels of transforming growth factor-β1 (TGF-β1) (A), smooth muscle actin-α (B), and total and phosphorylated Smad-3 (Ser425) (C) in the viable non-infarcted myocardia of the left ventricles (LVs) of all groups of rats. Data are expressed as mean ± SD of 6rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.

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  Fig. 8. Total protein levels of Smad7 (A) and bone morphogenetic protein-7 (BMP7) (B) in the viable non-infarcted myocardia of the left ventricles (LVs) of all groups of rats. Data are expressed as mean ± SD of 6 rats/groups. a: significantly different as compared to control rats, b: significantly different as compared to control + Quercetin (QUR)-treated rats; and c: significantly different as compared with the myocardial infarction (MI)-induced rats.