Total flavonoids from Abrus cantoniensis alleviate fatty liver hemorrhagic syndrome in laying hens by regulating inflammation, oxidative stress, and cecal metabolites and microbiota

鸡骨草中的总黄酮可通过调节炎症、氧化应激、盲肠代谢物和微生物群来缓解蛋鸡的脂肪肝出血综合征。

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Abstract

Fatty liver hemorrhagic syndrome (FLHS) is a metabolic disease in laying hens. Total flavonoids from Abrus cantoniensis (TFAC) comprise multiple bioactive compounds with potential benefits against FLHS. This study aimed to explore the effects and mechanism of TFAC in improving FLHS. Firstly, analysis by liquid chromatography-tandem mass spectrometry identified 20 flavonoid compounds in the TFAC, including vicenin-3 and acacetin. Subsequently, 144 laying hens at 28 weeks of age with similar body weight (1.45 ± 0.03 kg) were randomly divided into six groups (eight replicates per group and three hen per replicate, n = 8): a control group (standard diet), an FLHS model group (high-energy and low-protein diet), three TFAC-supplemented groups (0.25, 0.50, and 1.00 g/kg), and a positive control group (1.00 g/kg choline chloride). After a two-week acclimation, the formal experiment lasted four weeks. Total flavonoids from A. cantoniensis significantly alleviated FLHS-induced alterations by reducing excessive liver weight (P < 0.001) and abdominal fat weight (P < 0.001), and decreasing hepatic lipid accumulation (triacylglycerol, total cholesterol, and free fatty acids; P < 0.05) as well as serum lipid levels (triacylglycerol, total cholesterol, aspartate aminotransaminase, alanine aminotransferase, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol; P < 0.05). It also enhanced hepatic antioxidant capacity (total antioxidant capacity, superoxide dismutase, and glutathione peroxidase; P < 0.05) and attenuated inflammation (as shown by decreased levels of interleukin-6, nuclear factor kappa-B, and cyclooxygenase-2; P < 0.05). Moreover, TFAC regulated cecal metabolites and microbiota, especially increasing Se-methyl-L-selenocysteine (P = 0.043) and probiotic Akkermansia (P = 0.028), as well as elevating lithocholic acid-3-sulfate (P < 0.001) and isodeoxycholic acid (P = 0.020). Reverse transcription quantitative polymerase chain reaction showed that TFAC upregulated farnesoid X receptor (FXR; P = 0.017) and organic solute transporter-β (P = 0.038) in the ileum. Meanwhile, in the liver, FXR (P = 0.040) and small heterodimer partner (P < 0.001) were increased, and fatty acid synthase (P = 0.003) was inhibited. In conclusion, this study demonstrated that TFAC ameliorated FLHS through multiple mechanisms, including attenuating hepatic inflammation, enhancing antioxidant capacity, and modulating cecal metabolites and microbiota. These findings suggest the potential of TFAC as a feed additive for improving poultry liver health.

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