As a
metabolic disease,
fatty liver hemorrhagic syndrome (
FLHS) has become a serious concern in laying hens worldwide. Abrus cantoniensis Hance (AC) is a commonly used plant in
traditional medicine for
liver disease treatment. Nevertheless, the effect and mechanism of the decoction of AC (ACD) on
FLHS remain unclear. In this study, ultra-high performance liquid chromatography analysis was used to identify the main
phytochemicals in ACD.
FLHS model of laying hens was induced by a high-energy low-
protein (HELP) diet, and ACD (0.5, 1, 2 g ACD/hen per day) was given to the hens in
drinking water at the same time for 48 days. Biochemical blood indicators and histopathological analysis of the liver were detected and observed to evaluate the
therapeutic effect of ACD. Moreover, the effects of ACD on liver metabolomics and gut microbiota in laying hens with
FLHS were investigated. The results showed that four
phytochemicals, including
abrine,
hypaphorine,
vicenin-2, and
schaftoside, were identified in ACD. ACD treatment ameliorated biochemical blood indicators in laying hens with
FLHS by decreasing
aspartate aminotransferase,
alanine aminotransferase,
triglycerides,
low-density lipoprotein cholesterol, and total
cholesterol, and increasing
high-density lipoprotein cholesterol. In addition,
lipid accumulation in the liver and pathological damages were relieved in ACD treatment groups. Moreover, distinct changes in liver metabolic profile after ACD treatment were observed, 17 endogenous liver metabolites mainly associated with the metabolism of
arachidonic acid,
histidine,
tyrosine, and
tryptophan were reversed by ACD. Gut microbiota analysis revealed that ACD treatment significantly increased bacterial richness (Chao 1, P < 0.05; Ace, P < 0.01), and upregulated the relative abundance of Bacteroidetes and downregulated Proteobacteria, improving the negative effects caused by HELP diet in laying hens. Taken together, ACD had a protective effect on
FLHS by regulating blood
lipids, reducing liver
lipid accumulation, and improving the
dysbiosis of liver metabolomics and gut microbiota.