Simvastatin Significantly Reduced Alcohol-Induced Cardiac Damage in Adolescent Mice

Figures

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  Fig. 1. Representative photomicrographs of the H&E-stained sections a at a low magnification (Scale bar = 50 µm), b at a high magnification (Scale bar = 20 µm), the box plots of c the cardiomyocyte area, and d the cardiomyocyte diameter across the different experimental groups, for both sexes. The histology of the myocardium was typical of the normal histology found in the myocardium of mice. The cardiomyocytes were oval with distinct nuclei. In both sexes, the area or the diameter of cardiomyocytes was significantly higher in the ALC group than in the NT group, thus confirming alcohol-induced myocardial hypertrophy. Both concentrations of Simvastatin were effective against alcohol-induced myocardial hypertrophy in both sexes. No editing was done to the images. NT non-treatment, SIM 5-mg Simvastatin, ALC alcohol, ALC + SIM5 5-mg Simvastatin and alcohol, ALC + SIM15 15-mg Simvastatin and alcohol, NS not significant at P > 0.05

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  Fig. 2. Representative photomicrographs of the MT-stained sections a at a low magnification (Scale bar = 50 µm), b at a high magnification (Scale bar = 10 µm), and c the box plot of the percentage collagen distribution across the different experimental groups, for both sexes. Collagen deposition in the myocardium is indicated by black arrows. In both sexes, collagen distribution was significantly higher in the ALC group than in the NT group, thus confirming alcohol-induced myocardial fibrosis. Both Simvastatin concentrations significantly reduced alcohol-induced myocardial fibrosis except in the males where 15-mg Simvastatin had no beneficial effect—an indication of possible sex-specific differences in the effects of Simvastatin against alcohol-induced myocardial fibrosis. No editing was done to the images. NT non-treatment, SIM 5-mg Simvastatin, ALC alcohol, ALC + SIM5 5-mg Simvastatin and alcohol, ALC + SIM15 15-mg Simvastatin and alcohol, NS not significant at P > 0.05

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  Fig. 3. Representative photomicrographs of the TNF-α-immunolabelled sections a at a low magnification (Scale bar = 50 µm), b at a high magnification (Scale bar = 50 µm), and c the box plot of the percentage TNF-α distribution across the different experimental groups, for both sexes. Varying degrees of TNF-α expression are noticeable across the experimental groups. In both sexes, TNF-α distribution was significantly higher in the ALC group than in the NT group, thus confirming alcohol toxicity in the cardiomyocytes. Both concentrations of Simvastatin were effective against alcohol-induced myocardial inflammation. A lower Simvastatin concentration was effective in the females but not in the males—an indication of possible sex-specific differences in the effect of Simvastatin against alcohol effects on the cardiomyocytes. No editing was done to the images. NT non-treatment, SIM 5-mg Simvastatin, ALC alcohol, ALC + SIM5 5-mg Simvastatin and alcohol, ALC + SIM15 15-mg Simvastatin and alcohol, NS not significant at P > 0.05