Astaxanthin supplementation mitigated intestinal damage and immunity in overfed Pekin ducks by regulating gut morphology, intestinal inflammation, and antioxidant balance

虾青素补充剂通过调节肠道形态、肠道炎症和抗氧化平衡,减轻了过度喂养的北京鸭的肠道损伤并增强了其免疫力。

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Abstract

This study explored the impact of astaxanthin (AST) supplementation on growth performance, serum lipid profile, gut morphology, and antioxidant and immune function in the intestinal mucosa of Pekin ducks subjected to overfeeding. A total of 150 male Pekin ducks at one day of age were randomly allotted into five treatment groups with five replicates of six ducks each. The control group and ad libitum group (ALG) received a basal diet while others received basal diets supplemented with AST at 40 mg/kg (Low-dose group [LDG]), 80 mg/kg (medium-dose group [MDG]), and 120 mg/kg (high-dose group [HDG]). After 1 to 14 d on basal diets (brooding phase), the ducks were assigned to the dietary treatment groups for 15 to 38 d (Grower phase) and 39 to 42 d (overfeeding period). Results indicated that AST supplementation improved final body weight and weight gain at both the grower and overfeeding phases (P < 0.05). Overfeeding increased the serum lipid level, altered intestinal morphology, and led to higher expression of pro-inflammatory factors and oxidative stress biomarkers while reducing antioxidant enzyme activity, associated gene expression, and anti-inflammatory factors in the duodenal and jejunal mucosa (P < 0.05). Additionally, overfeeding caused increased apoptotic cell counts in the duodenal and jejunal mucosa of the control group (P < 0.05), culminating in intestinal tissue damage and dysfunction. Dietary supplementation of AST mitigated these adverse effects, alleviated intestinal damage and promoted gut health. It exerted a hypolipidemic effect, improved villi morphometrics in the duodenum, jejunum, and ileum, and enhanced the levels of interleukin-4 (IL-4), soluble tumor necrosis factor-alpha receptor (sTNFαR), and transforming growth factor-beta (TGF-β) (P < 0.05). It also increased the activities of antioxidant enzymes and the mRNA expression of key antioxidant-related genes, including nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione S-transferases (GSTs), and glutamate-cysteine ligase catalytic subunit (GCLC) (P < 0.05). Moreover, it reduced the expression of pro-inflammatory factors, oxidative stress biomarkers such as reactive oxygen species (ROS) and malondialdehyde (MDA), and the number of apoptotic cells in the duodenal and jejunal mucosa (P < 0.05). Immunoglobulin secretion and mucosal immunity were also significantly improved with AST supplementation (P < 0.05). Variations among the AST dietary groups suggest that a medium dosage of 80 mg/kg could effectively mitigate intestinal damage from overfeeding while enhancing growth performance, antioxidant defences, and immune responses. Our results would provide a theoretical reference for using AST as a nutritional strategy to enhance gut health in ducks exposed to overfeeding.

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