BACKGROUND: The aim of this study was to evaluate the preventive and therapeutic potential of hyperbaric oxygen therapy (HBO) on the liver tissue against bile duct ligation (BDL)-induced oxidative damage and fibrosis in rats. MATERIALS AND METHODS: We divided 32 adult male Sprague Dawley rats into four groups: sham, sham plus HBO, BDL, and BDL plus HBO; each group contained eight animals. We placed the sham plus HBO and BDL plus HBO groups in an experimental hyperbaric chamber in which we administered pure oxygen at 2.5 atmospheres absolute 100% oxygen for 90 min on 14 consecutive days. RESULTS: The application of BDL clearly increased the tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and decreased the antioxidant enzymes (superoxide dismutase and catalase activities) and glutathione level. Hyperbaric oxygen therapy treatment significantly decreased the elevated tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and increased the reduced superoxide dismutase and catalase activities and glutathione level in the tissues. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with HBO attenuated alterations in liver histology. Alpha smooth muscle actin, cytokeratin-positive ductular proliferation, and the activity of terminal deoxynucleotidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling in the BDL decreased with HBO treatment. CONCLUSIONS: The data indicate that HBO attenuates BDL-induced oxidative injury, hepatocytes damage, bile duct proliferation, and fibrosis. The hepatoprotective effect of HBO is associated with antioxidative potential.
BACKGROUND: The aim of this study was to evaluate the preventive and therapeutic potential of hyperbaric oxygen therapy (HBO) on the liver tissue against bile duct ligation (BDL)-induced oxidative damage and fibrosis in rats. MATERIALS AND METHODS: We divided 32 adult male Sprague Dawley rats into four groups: sham, sham plus HBO, BDL, and BDL plus HBO; each group contained eight animals. We placed the sham plus HBO and BDL plus HBO groups in an experimental hyperbaric chamber in which we administered pure oxygen at 2.5 atmospheres absolute 100% oxygen for 90 min on 14 consecutive days. RESULTS: The application of BDL clearly increased the tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and decreased the antioxidant enzymes (superoxide dismutase and catalase activities) and glutathione level. Hyperbaric oxygen therapy treatment significantly decreased the elevated tissue malondialdehyde level, myeloperoxidase activity, and hydroxyproline content and increased the reduced superoxide dismutase and catalase activities and glutathione level in the tissues. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with HBO attenuated alterations in liver histology. Alpha smooth muscle actin, cytokeratin-positive ductular proliferation, and the activity of terminal deoxynucleotidyl transferase 2'-deoxyuridine, 5'-triphosphate nick end labeling in the BDL decreased with HBO treatment. CONCLUSIONS: The data indicate that HBO attenuates BDL-induced oxidative injury, hepatocytes damage, bile duct proliferation, and fibrosis. The hepatoprotective effect of HBO is associated with antioxidative potential.