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AIM: To study the protective effects and mechanisms of Se-enriched lactobacillus on liver injury caused by carbon tetrachloride(CCI_4) in mice. METHODS: Seventy-two ICR mice were randomly divided into four groups: normal group, CCl_4-induced model group, low Se-enriched lactobacillus treatment group(L-Se group), and high Se-enriched lactobacillus treatment group(H-Se group). During a 3-wk experimental period, the common complete diet was orally provided daily for normal group and model group, and the mice in L-Se and H-Se groups were given a diet with 2 and 4 mg of organoselenium from Se-enriched lactobacillus per kg feed, respectively. From the 2~(nd) wk of experiment, the model group, L-Se group, and H-Se group received abdominal cavity injection of olive oil solution containing 500 mL/L CCl_4(0.07 mL/100 g body mass) to induce liver injury, and the normal group was given olive oil on every other day for over 2 wk. In the first 2 wk post injection with CCl_4, mice in each group were killed. The specimens of blood, liver tissue, and macrophages in abdominal cavity fluid were taken. Then the activities of the following liver tissue injury-associated enzymes including glutathione peroxidase(GSH-Px), superoxide dismutase(SOD), alanine aminotransferase(ALT) and aspartate aminotransferase(AST) as well as malondialdehyde(MDA) content were assayed. Changes of phagocytic rate and phagocytic index in macrophages were observed with Wright-Giemsa stain. Plasma TNF-α level was measured by radioimmunoassay. The level of intracellular free Ca~(2+)([Ca~(2+)]_i) in hepatocytes was detected under a laser scanning confocal microscope. RESULTS: During the entire experimental period, the AST and ALT activities in liver were greatly enhanced by CCl_4 and completely blunted by both low and high doses of Se-enriched lactobacillus. The Se-enriched lactobacillusprotected liver homogenate GSH-Px and SOD activities were higher or significantly higher than those in model group and were close to those in normal group. CCl_4 significantly increased MDA content in liver homogenates, while administration of Se-enriched lactobacillus prevented MDA elevation. Phagocytic rate and phagocytic index of macrophages decreased after CCl_4 treatment compared to those in normal control, but they were dramatically rescued by Se-enriched lactobacillus, showing a greatly higher phagocytic function compared to model group. CCl_4 could significantly elevate plasma TNF-α and hepatocyte[Ca~(2+)]_i level, which were also obviously prevented by Se-enriched lactobacillus. CONCLUSION: Se-enriched lactobacillus can intervene in CCl_4-induced liver injury in mice by enhancing macrophage function activity to keep normal and beneficial effects, elevating antioxidant-enzyme activities and reducing lipid peroxidation reaction, inhibiting excessive release of TNF-α, preventing the dramatic elevation of [Ca~(2+)]_i in hepatocytes.
AIM: To study the protective effects and mechanisms of Se-enriched lactobacillus on liver injury caused by carbon tetrachloride (CCI_4) in mice. METHODS: Seventy-two ICR mice were differentiated into four groups: normal group, CCl_4- induced model group, low Se-enriched lactobacillus treatment group (L-Se group), and high Se-enriched lactobacillus treatment group (H-Se group) group, and the mice in L-Se and H-Se groups were given a diet with 2 and 4 mg of organoselenium from Se-enriched lactobacillus per kg feed, respectively. From the 2 ~ (nd) wk of experiment, the model group , L-Se group, and H-Se group received abdominal cavity injection of olive oil solution containing 500 mL / L CCl_4 (0.07 mL / 100 g body mass) to induce liver injury, and the normal group was given olive oil on every other day for over 2 wk. In the first 2 wk post injection with CCl_4, mice in each group were The activities of the following liver tissue injury-associated enzymes including glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), alanine aminotransferase (ALT Changes in phagocytic rate and phagocytic index in macrophages were observed with Wright-Giemsa stain. Plasma TNF-α level was measured by radioimmunoassay. The level of intracellular free RESULTS: During the entire experimental period, the AST and ALT activities in liver were greatly enhanced by CCl_4 and completely blunted by both low and high doses of Se-enriched lactobacillus. The Se-enriched lactobacillusprotected liver homogenate GSH-Px and SOD activities were higher or significantly higher than those in model group and were closeCCl_4 significantly increased MDA content in liver homogenates, while administration of Se-enriched lactobacillus prevented MDA elevation. Phagocytic rate and phagocytic index of macrophages decreased after CCl_4 treatment compared to those in normal control, but they wereapest rescued by Se-enriched lactobacillus, showing a greatly enhanced phagocytic function compared to model group. CCl_4 could significantly elevate plasma TNF-α and hepatocyte [Ca ~ (2 +)] _ i level, which were also prevented substantially by Se-enriched lactobacillus. CONCLUSION: Se-enriched lactobacillus can intervene in CCl_4-induced liver injury in mice by enhancing macrophage function activity to keep normal and beneficial effects, elevating antioxidant-enzyme activities and reducing lipid peroxidation reaction, inhibiting excessive release of TNF-α, preventing the dramatic elevation of of [Ca ~ (2 +)] _i in hepatocytes.