Molecular mechanism of homologous lactic acid bacteria regulating liver cell injury of snakehead fish

Abstract

In order to clarify the molecular mechanism of the homologous LAB regulating the liver cell injury of C. argus, this study used Fxr as the key target protein for the treatment of liver cell injury, used LCA to construct the liver cell injury model, and used the Fxr inhibitor GS to specifically block Fxr and its related signaling pathways will further explore the protective mechanism of homologous L. lactis L19 against liver injury in C. argus in vitro. The results showed that the LCA-induced liver cell injury model of C. argus was successfully constructed. The optimal concentration of LCA was 20 μM, and the optimal duration of action was 24 h. 1.0 × 108 CFU/mL L. lactis L19 ECP showed a protective effect on LCA-induced liver cell injury, remarkably decrease the levels of liver injury-related biochemical parameters AST, ALT, ALP and LDH (P < 0.05), and regulate the expressions of BA metabolism-related genes fxr, bsep, mrp2, shp, cyp7a1 and cyp8b1 and BA metabolism-related proteins Fxr, Bsep, Shp and Cyp7a1. It is revealed that L. lactis L19 is a possible molecular mechanism that regulates the liver cell injury of C. argus by activating Fxr and its related signal pathways. In vitro test results show that L. lactis L19 can enhance the proliferation of hepatocytes, promote the efflux and metabolism of toxic BA, inhibit the BA synthesis and uptake, and play a protective role in LCA-induced liver cell injury in C. argus. At the gene and protein levels, it was verified that L. lactis L19 can activate Fxr and its related signal pathways, and proved that the protective effects of L. lactis L19 on LCA-induced liver cell injury was blocked by GS. Thus, L. lactis L19, as a recognized probiotic, has a bright future in the treatment of liver injury-related diseases.