4.7 Article

Effects of Dietary Supplementation of Algae-Derived Polysaccharides on Morphology, Tight Junctions, Antioxidant Capacity and Immune Response of Duodenum in Broilers under Heat Stress

Journal

ANIMALS
Volume 11, Issue 8, Pages -

Publisher

MDPI
DOI: 10.3390/ani11082279

Keywords

broilers; seaweed polysaccharides; heat stress; intestinal health; signaling pathway

Funding

  1. Natural Science Foundation of Guangdong Province of China [2018A030307023]
  2. National Nature Science Foundation of China [32002196]
  3. College Student Innovation Training Program [S202110566027]

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This study demonstrated that dietary supplementation of algae-derived polysaccharides (ADP) improved the duodenal health of broilers under heat stress (HS) by enhancing tight junction expression, antioxidant capacity, and modulating the immune response. These beneficial effects of ADP supplementation may be attributed to the regulation of Nrf2 and NF-kappa B signaling pathways.
Simple Summary Heat stress (HS) has become a great challenge for poultry production in tropical and subtropical regions. HS results in the intestinal dysfunction of broilers, which seriously affects their productivity. Our previous study suggested that dietary supplementation of algae-derived polysaccharides (ADP) could promote the intestinal barrier function in broilers, but the effect of dietary ADP supplementation on the intestinal health of broilers under HS remains unclear. The present study showed that dietary ADP supplementation improved the duodenal tight junction expression of broilers under HS, and found that dietary ADP mitigated HS-induced oxidative stress and inflammation response by regulating Nrf2 and NF-kappa B signaling pathways. These findings reveal the potential application of ADP as an HS-alleviating agent to maintain gut health in broilers. To evaluate the ameliorative effect of algae-derived polysaccharide (ADP) supplementation on duodenal injury caused by heat stress (HS) in broilers, a total of 144 male yellow-feathered broilers (56-day-old) were randomly allocated into three groups: The TN group (thermoneutral zone, broilers were raised at 23.6 +/- 1.8 degrees C); HS group (heat stress, broilers were exposed to 33.2 +/- 1.5 degrees C 10 h/day, 8:00 a.m.-18:00 p.m., the temperature in the remaining period was consistent with the TN group); HSA group (heat-stressed broilers were fed with ADP supplemented diet at 1000 mg/kg). There were six replications in each treatment, and eight broilers in each replication. The feeding trial lasted four weeks. The results showed that dietary ADP supplementation tended to increase the villus height (p = 0.077) and villus width (p = 0.062), and decrease the apoptosis rate (p = 0.081) in the duodenum of broilers under HS. Furthermore, dietary ADP increased the relative mRNA and protein (based on immunofluorescence) expression levels of occludin and zonula occludens-1 (ZO-1) in the duodenum of broilers under HS (p < 0.05). In addition, dietary ADP enhanced the total antioxidation capacity (T-AOC) and activity of glutathione-S transferase (GST), while reducing the malondialdehyde (MDA) concentration of the duodenum in broilers under HS (p < 0.05). Moreover, dietary ADP supplementation upregulated the duodenal nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), glutathione peroxidase 1 (GPx1) and glutathione S-transferase theta 1 (GSTT1) mRNA expression levels in heat-stressed broilers (p < 0.05). Furthermore, compared with the HS group, broilers fed with an ADP supplemented diet had a higher relative mRNA expression of inhibitor kappa B alpha (I kappa B alpha) (p < 0.05) and a lower relative mRNA expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) in the duodenum (p < 0.05). In summary, dietary ADP supplementation had an ameliorative effect on HS-induced impairment of tight junctions, antioxidant capacity and the immune response of the duodenum in broilers. These beneficial effects might be related to the modulation of Nrf2 and NF-kappa B signaling pathways.

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