@article {10.3844/ojbsci.2014.12.20,
article_type = {journal},
title = {TAURINE ATTENUATES HEPATIC AND CARDIAC DAMAGE AND APOPTOSIS IN RABBITS FED A HIGH-FAT DIET},
author = {Abdel-Rahman, Gamal Hasan},
volume = {14},
number = {1},
year = {2013},
month = {Dec},
pages = {12-20},
doi = {10.3844/ojbsci.2014.12.20},
url = {https://thescipub.com/abstract/ojbsci.2014.12.20},
abstract = {A hypercholesterolemia diet has been associated with the hepatic and cardiac abnormalities and the pathological changes. The present work was designed to investigate the histological and immunohistochemical changes in the liver and heart of rabbits when fed high fat diet and the possible protective role of an antioxidant "taurine". Twenty-four male white New Zealand rabbits were divided into four groups, 6 rabbits each. Group 1, served as a control, rabbits fed with a normal diet. Group 2, (taurine group), rabbits were given orally taurine (10 mg Kg-1 b.w/day) for 8 weeks. Group 3 (hypercholesterolemic group), rabbits fed (2% cholesterol-enriched diet for 8 weeks. Group 4, rabbits fed 2% cholesterol-enriched diet plus taurine (10 mg Kg-1 b.w/day) orally for the same period. Histopathological examinations revealed that high cholesterol diet caused hepatic and myocardial tissue changes compared with rabbits fed with a normal diet. Including fatty degeneration, inflammations and necrosis of Hepatocytes and vacuolar degeneration, disorganization of myofibrils and necrosis of myocardial cells. Immunohistochemistry for caspase-3 for apoptosis were performed. Caspase-3 positive cells in the liver tissue and Caspase-3 positive area in myocardial tissue increased in high cholesterol diet group. Taurine markedly attenuate hypercholesterolemia-induced cardiac and hepatic histopathological changes in the cholesterol plus taurine group compared to the cholesterol group. Thus, the results suggest that taurine could play a beneficial role against hypercholesterolemia-induced complications in the liver and heart of the rabbits.},
journal = {OnLine Journal of Biological Sciences},
publisher = {Science Publications}
}