Silymarin mediates the gut-liver axis pathway to alleviate Carassius auratus hepatic lipid metabolism disorders caused by carbonate exposure

Abstract

An 8-week feeding trial was conducted to investigate the mechanism of silymarin alleviating the abnormal lipid metabolism of Hefang Crucian Carp (HCC) (13.43 ± 0.059 g) liver caused by carbonate exposure. The fish were randomly divided into three groups: Control group (group B, 0 g/L carbonate, 0 mg/kg silymarin), carbonate stress group (group CA, 3 g/L carbonate, 0 mg/kg silymarin) and silymarin group (group SI, 3 g/L carbonate, 60 mg/kg silymarin). The results showed that the growth performance of group CA was significantly increased compared with group B. Compared with CA group, brush villi in SI group recovered significantly, and the width of submucosa decreased. Compared with group B, the intestinal barrier was damaged and permeability increased in group CA, while the damage was alleviated in group SI. Intestinal microbiota analysis showed that the bacterial community function genes related to lipopolysaccharide biosynthesis protein and lipopolysaccharide biosynthesis in CA group were higher than those in B and SI groups, and it was found that the change of LPS content in fish was echoed by the results of intestinal microflora. Compared with group B, the liver of group CA was damaged and the lipid metabolism process was abnormal, resulting in lipid metabolism disorder. SI group alleviated the liver damage caused by carbonate exposure, promoted the process of liver lipid synthesis, and balanced the body's lipid metabolism. More than 50 % of the metabolites are closely related to lipids and lipid molecules. The most metabolites in metabolism are oxidative phosphorylation and pyruvate metabolism. In summary, this study demonstrated that silymarin alleviating carbonate exposure altered intestinal microbiota homeostasis in HCC, leading to intestinal inflammation and increased mucosal barrier permeability, inhibiting LPS synthesis and absorption, preventing it from entering the liver through the intestinal liver, and increasing oxidative stress in the liver and abnormal lipid metabolism in the liver, thereby leading to liver injury. To provide theoretical basis for the development and utilization of silymarin functional feed additives and the mitigation strategy of carbonate exposure to liver damage in fish.