The aim of this study was to investigate the effect of dietary resveratrol supplementation on innate immunity and inflammatory responses in the spleen of yellow-feather broilers under heat stress. A total of 288 yellow-feather broilers of 28-day-old were randomly assigned to 3 treatment groups with 6 replicates. A thermo-neutral group (TN) (24 ± 2°C) received a basal diet and another 2 heat-stressed groups (37 ± 2°C for 8 h/D and 24 ± 2°C for the remaining time) were fed the basal diet (HT) or basal diet with 500 mg/kg resveratrol (HT+Res) for 14 consecutive days. The results showed that heat stress decreased (P < 0.05) the growth index of thymus, spleen, and bursa of Fabricius, reduced (P < 0.05) the levels of complement C3 and C4 in serum. Heat stress also caused activation of inflammatory immune responses evidenced by increased (P < 0.05) the mRNA abundance of HSP (heat shock protein) 70, toll-like receptor (TLR)1, TLR4, TLR5, myeloid differentiation factor-88 (MyD88), nucleotide-binding oligomerization domain 1 (NOD1), Dectin-1, transforming growth factor-β-activated kinase 1 (TAK1), interleukin (IL)-1, IL-4, IL-6, and tumor necrosis factor (TNF)-α, but decreased the mRNA abundance of interferon (IFN)-γ, activated nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPK), and phosphoinositide-3 kinases-protein kinase B (PI3K/AKT) signaling pathways. Dietary supplementation with resveratrol improved (P < 0.05) the growth index of thymus, spleen and bursa Fabricius, and increased (P < 0.05) the serum level of complement C3 under heat stress. In addition, resveratrol reduced (P < 0.05) the mRNA abundance of HSP70, TLR4, TLR5, NOD1, Dectin-1, and TAK1, and inhibited the NF-κB, MAPK and PI3K/AKT signaling pathway via down-regulated the phosphorylation of p65, extracellular signal-regulated kinases 1/2, c-Jun N-terminal protein kinase and AKT, as well as decreased the inflammatory cytokines expression, including IL-1, IL-4, IL-6, and TNF-α in the spleen under heat stress. Collectively, dietary resveratrol could have beneficial effects to regulate innate immunity and inflammatory response, via inhibiting the activation of NF-κB, MAPK, and PI3K/AKT signaling pathways induced by heat stress in the spleen.

中文翻译：

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膳食白藜芦醇补充剂可抑制黄羽肉鸡脾脏中热应激诱导的高活化先天免疫和炎症反应。

本研究旨在探讨日粮中添加白藜芦醇对热应激下黄羽肉鸡脾脏先天免疫和炎症反应的影响。将28日龄黄羽肉鸡288只随机分配到3个处理组，6个重复。一个热中性组 (TN) (24 ± 2°C) 接受基础饮食，另外 2 个热应激组（37 ± 2°C 8 小时/天，24 ± 2°C 剩余时间）喂食基础饮食 (HT) 或基础饮食与 500 mg/kg 白藜芦醇 (HT+Res) 连续 14 天。结果表明，热应激降低（P < 0.05）胸腺、脾脏和法氏囊的生长指数，降低（P < 0.05）血清补体C3和C4水平。热应激还引起炎症免疫反应的激活，表现为增加（P < 0. 05）HSP（热休克蛋白）70、toll样受体（TLR）1、TLR4、TLR5、骨髓分化因子88（MyD88）、核苷酸结合寡聚结构域1（NOD1）、Dectin-1的mRNA丰度，转化生长因子-β-活化激酶 1 (TAK1)、白细胞介素 (IL)-1、IL-4、IL-6 和肿瘤坏死因子 (TNF)-α，但降低了干扰素 (IFN)-γ 的 mRNA 丰度、活化核因子 kappa B (NF-κB)、丝裂原活化蛋白激酶 (MAPK) 和磷酸肌醇 3 激酶-蛋白激酶 B (PI3K/AKT) 信号通路。白藜芦醇的膳食补充改善了（P < 0.05）胸腺、脾脏和法氏囊的生长指数，并增加了（P < 0.05）热应激下补体C3的血清水平。此外，白藜芦醇降低 (P < 0.05) HSP70、TLR4、TLR5、NOD1、Dectin-1 和 TAK1 的 mRNA 丰度，并通过下调 p65、胞外信号调节激酶 1/2、c-Jun N-末端蛋白激酶和 AKT 的磷酸化，以及降低炎性细胞因子来抑制 NF-κB、MAPK 和 PI3K/AKT 信号通路热应激下脾脏中 IL-1、IL-4、IL-6 和 TNF-α 的表达。总的来说，膳食白藜芦醇可以通过抑制脾脏中热应激诱导的 NF-κB、MAPK 和 PI3K/AKT 信号通路的激活来调节先天免疫和炎症反应。和热应激下脾脏中的TNF-α。总的来说，膳食白藜芦醇可以通过抑制脾脏中热应激诱导的 NF-κB、MAPK 和 PI3K/AKT 信号通路的激活来调节先天免疫和炎症反应。和热应激下脾脏中的TNF-α。总的来说，膳食白藜芦醇可以通过抑制脾脏中热应激诱导的 NF-κB、MAPK 和 PI3K/AKT 信号通路的激活来调节先天免疫和炎症反应。