ABSTRACT
OBJECTIVE: To study the effect of selenium-enriched Bifidobacterium longum on alcoholic liver damage and its mechanism. METHODS: Alcoholic liver damage of female C57/BL6 mice were induced with 20% alcohol for 42 d, at the same time 50 or 100 mg•kg-1 selenium-enriched Bifidobacterium longum were administrated respectively. Mice livers were collected for calculating liver index, HE staining and measuring liver tissue malondialdehyde (MDA) and superoxide dismutase (SOD) level. Serum were collected for measurement of alanine transarninase (ALT), aspartate aminotransferase (AST),γ-glutamyltransferase (GGT) and tumor necrosis factor α (TNF-α) levels. The mRNA levels of liver SREBP-1c, AMPK and PPAR-α were measured with Real-time PCR. RESULTS: Selenium-enriched Bifidobacterium longum inhibited the increase in liver index and inflammation index induced with alcohol. Selenium-enriched Bifidobacterium longum also inhibited alcohol induced ALT, AST, GGT and TNF-α levels increase; decreased liver MDA levels and increased liver SOD levels. Selenium-enriched Bifidobacterium longum down-regulated SREBP-1c mRNA and up-regulated AMPK and PPAR-α mRNA levels of mice liver. CONCLUSION: Selenium-enriched Bifidobacterium longum protects mice from alcohol induced liver damage in a dose dependent manner. Its protective mechanism might be anti-oxidation, inflammation inhibition and improvement of lipid metabolism.
ABSTRACT
To investigate the protective effect of selenium-enriched Bifidobacterium longum preparation on rat IEC6 cells via the application of lipopolysaccharide (LPS)-induced IEC6 cell injury model. Methods The experiment was divided into five groups; negative control group treated with phosphoric acid equilibrium salt solution, model group treated with LPS, and low, medium, high concentration group in which IEC6 cells were treated with LPS plus 10, 30, 100 mg • L"1 water-soluble proteins from selenium-enriched Bifidobacterium longum respectively. After treatment with LPS for 24 hours, IEC6 cell viability, apoptosis, mitochondria membrane potential, and the expression of zonula occludens 1 (ZO-1) and Occludin were detected. Results LPS induced rat intestinal epithelial cell damage, such as the decrease of cell viability, the increase of cell apoptosis, the collapse of mitochondria membrane potential, and the decrease of cell tight junction protein expression. Water-soluble proteins from selenium-enriched Bifidobacterium longum inhibited LPS-induced IEC6 cell damage, decreased cell apoptosis and increased cell tight junction between cells. Conclusion Water-soluble proteins from selenium-enriched Bifidobacterium longum have protective effect on LPS-induced rat intestinal epithelial cell injury.