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  • Title: Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by D-galactosamine.
    Author: Kasravi FB, Adawi D, Molin G, Bengmark S, Jeppsson B.
    Journal: J Hepatol; 1997 Feb; 26(2):417-24. PubMed ID: 9059965.
    Abstract:
    BACKGROUND/AIM: Bacterial infections and sepsis are frequent complications of acute liver injury, with a high share in the mortality and morbidity of this condition. Bacterial translocation from the gut may play an important role in the high rate of infections observed. In this experiment the effect of different oral supplementation on bacterial translocation was evaluated in acute liver injury induced by D-galactosamine in the rat. METHODS: Rats were given oral supplements of lactulose, neomycin, Lactobacillus reuteri R2LC, and Lactobacillus plantarum DSM 9843 for 1 week. Liver injury was induced by intraperitoneal administration of 1.1 g/kg D-galactosamine. Twenty-four hours later, rats were sacrificed and liver enzymes and histology, intestinal bacterial count and microflora, intestinal mucosal histology, DNA and RNA content, bacterial translocation to blood, mesenteric lymph nodes, and liver, and serum endotoxin were studied or measured. RESULTS: Lactulose was highly effective in prevention of liver injury and bacterial translocation. Neomycin and Lactobacillus plantarum DSM 9843 showed a moderate effect in prevention of liver injury and bacterial translocation. Intestinal bacterial count and microflora were affected by different treatment modalities. No endotoxin concentration was found in any of the experimental groups. Both lactobacilli could significantly improve the mucosal proliferative state. CONCLUSIONS: Oral supplementation of lactulose with anti-endotoxin effect could successfully prevent the liver injury and the subsequent bacterial translocation in acute liver injury induced by administration of D-galactosamine in the rat. This effect was irrespective of the intestinal bacterial alteration or mucosal proliferative state.
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