BCAA protect the liver from cirrhotic injury via suppression of LBP-TLR4-STAT3 activation and E. faecalis translocation

Abstract Objectives : Branched-chain amino acids (BCAA) are used as nutritional support and improving prognosis in liver cirrhosis (LC). Here we investigate the molecular mechanisms of BCAA treatment and liver damage focused on liposaccharide binding protein (LBP) related pathways. Methods : Serum LBP levels were measured in cirrhotic patients and in cirrhotic rats treated with BCAA to examine the correlation between liver function and survival. In cirrhotic rats, liver damage, enterococcus faecalis (Ef) translocation, serum capsular polysaccharide (CPS) and intestinal tight junction levels were assessed. Damaged HepG2 cells were cultured with BCAA-supplemented, BCAA-deficient, or control amino acid medium, followed by examining LBP expression. Results : Serum LBP levels were significantly increased in deceased LC patients. The survival rate in patients with lower serum LBP ( Conclusions : Serum LBP level is a prognostic biomarker in LC. BCAA treatment reduced translocation of Ef through intestinal tight junction recovery and reduced LBP expression in the liver, which repressed LBP-TLR4-STAT3 activation. Our findings suggest that BCAA supplementation protects the liver from damage via multiple pathways.