| Objective:This work aimed to screen bifidobacteria which can prevent or attenuate acute liver injury and reveal the mechanism.Methods:Fifteen strains of bifidobacteria were isolated from the stool samples of healthy adults under anaerobic condition.From these,five strains,including Bif-LI06,Bif-LI07,Bif-LI08,Bif-LI09 and Bif-LI 10,were picked up referring to a number of articles.These strains were given to five groups of Sprague-Dawley rats respectively by gavages for 7 days(3x109CFU/ml,lml/day).Meanwhile,positive controls and negative controls were given the same amount of normal saline for 7 days.Acute liver injury was induced on the 8th day by an intraperitoneal injection of 1.1 g/kg body weight of D-galactosamine.After 24 hours,samples were collected to determine the liver function,histology of liver and terminal ileum,composition of the gut microbiome,bacterial translocation and plasma levels of cytokines which can assess the effect of each bifidobacterium strain and explain the mechanism to some extent.Results:The results indicated that pretreatment with Bif-LI09 or Bif-LI10 significantly reduced elevated alanine aminotransferase(ALT)and aspartate aminotransferase(AST)levels and reduced liver histological abnormalities.While pretreatment with LI06,Bif-LI07 or Bif-LI08 did not demonstrate so significant effects during this process.Further study showed administration with Bif-LI09 or Bif-LI10 both resulted in a cecal microbiome which partly returned to normal,reduced histological abnormalities of terminal ileum,decreased bacterial translocation(BT)and significantly decreased the plasma level of macrophage colony stimulating factor(M-CSF),macrophage inflammatory protein 1 alpha(MIP-1α)and monocyte chemotactic protein 1(MCP-1).Conclusion:Both Bif-LI09 and Bif-LI10 can greatly improve acute liver injury induced by D-Galactosamine,which enable them to serve as potential probiotics for the prevention or treatment of acute liver injury.The mechanism involves regulating the gut microbiome,protecting the gut barrier and inhibiting the exaggerated inflammatory response. |