Selenium Supplementation Decreases Hepatic Fibrosis in Mice After Chronic Carbon Tetrachloride Administration
2010
Ding, Ming | Potter, James J. | Liu, Xiaopu | Torbenson, Michael S. | Mezey, Esteban
Oxidative stress stimulates fibrogenesis, and selenium (Se) has antioxidant properties. This study determined whether Se supplementation affects CCl₄-induced liver injury and fibrosis. Mice were administered CCl₄ over 4 weeks, while controls received olive oil. Se was provided as sodium selenite in the drinking water. Se increased liver Se-dependent glutathione peroxidase activity and decreased liver malondialdehyde after CCl₄. Se decreased liver inflammation but not necrosis caused by CCl₄. Se increased hepatocyte apoptosis after CCl₄ and the pro-apoptotic BAX and Bcl Xs/l proteins. Stellate cell apoptosis occurred only after CCl₄ in Se-supplemented mice. Se decreased stellate cell number and fibrosis after CCl₄. Liver matrix metalloproteinase-9 increased after CCl₄ with Se supplementation. In conclusion, Se supplementation decreased hepatic fibrosis after CCl₄ in the setting of decreased inflammation but increased apoptosis. The principal mechanisms for the decreased fibrosis are a lower number of collagen-producing stellate cells and increased collagen degradation.
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