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饲粮添加白藜芦醇抑制热应激诱导的黄羽肉鸡脾脏中高活化固有免疫和炎症反应。

Dietary resveratrol supplementation inhibits heat stress-induced high-activated innate immunity and inflammatory response in spleen of yellow-feather broilers.

机构信息

College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China.

出版信息

Poult Sci. 2019 Dec 1;98(12):6378-6387. doi: 10.3382/ps/pez471.

DOI:10.3382/ps/pez471
PMID:31406997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8913767/
Abstract

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.

摘要

本研究旨在探讨饲粮补充白藜芦醇对热应激条件下黄羽肉鸡脾脏固有免疫和炎症反应的影响。将 288 只 28 日龄黄羽肉鸡随机分为 3 个处理组,每个处理组设 6 个重复。常温组(TN)(24±2℃)饲喂基础饲粮,另外 2 个热应激组(37±2℃持续 8 h/d,其余时间 24±2℃)分别饲喂基础饲粮(HT)或基础饲粮添加 500 mg/kg 白藜芦醇(HT+Res),连续饲喂 14 d。结果表明,热应激降低了(P<0.05)胸腺、脾脏和法氏囊的生长指数,降低了(P<0.05)血清补体 C3 和 C4 的水平。热应激还导致炎症免疫反应被激活,表现为热休克蛋白(HSP)70、Toll 样受体(TLR)1、TLR4、TLR5、髓样分化因子-88(MyD88)、核苷酸结合寡聚化结构域 1(NOD1)、Dectin-1、转化生长因子-β激活激酶 1(TAK1)、白细胞介素(IL)-1、IL-4、IL-6 和肿瘤坏死因子(TNF)-α的 mRNA 丰度增加(P<0.05),干扰素(IFN)-γ、激活核因子 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)信号通路的 mRNA 丰度降低(P<0.05)。饲粮补充白藜芦醇提高了(P<0.05)热应激条件下胸腺、脾脏和法氏囊的生长指数,增加了(P<0.05)血清补体 C3 的水平。此外,白藜芦醇降低了(P<0.05)HSP70、TLR4、TLR5、NOD1、Dectin-1 和 TAK1 的 mRNA 丰度,通过下调 p65、细胞外信号调节激酶 1/2、c-Jun N-末端蛋白激酶和 AKT 的磷酸化,抑制 NF-κB、MAPK 和 PI3K/AKT 信号通路,降低了热应激条件下脾脏中炎症细胞因子的表达,包括白细胞介素(IL)-1、IL-4、IL-6 和 TNF-α。综上所述,饲粮补充白藜芦醇通过抑制热应激诱导的 NF-κB、MAPK 和 PI3K/AKT 信号通路的激活,对固有免疫和炎症反应具有有益的调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/f6dd00dc3552/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/f74cc022fb22/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/2bce3fdbaedc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/fc3bdec74a83/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/c5df5968823f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/f6dd00dc3552/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/f74cc022fb22/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/2bce3fdbaedc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/fc3bdec74a83/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/c5df5968823f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b001/8913767/f6dd00dc3552/gr5.jpg

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