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饲粮添加色氨酸对热应激肉鸡肝脏、肠道抗氧化能力和炎症反应的影响 被引量:7

Effects of dietary tryptophan supplementation on antioxidant capacity and inflammatory response in liver and intestine of broilers subjected to heat stress
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摘要 本试验旨在研究饲粮添加色氨酸(Trp)对热应激(HS)肉鸡肝脏、肠道抗氧化能力和炎症反应以及相关信号通路的调节作用。选取180只健康体质量接近的18日龄雌性AA肉鸡,随机分为3个处理组,每组6个重复,每个重复10只鸡。适应性饲养3 d后,于21日龄开始进行温度控制,试验期为21 d。适温组(TN)肉鸡饲养于正常温度(23±1)℃,饲喂基础饲粮;热应激组(HS)肉鸡饲养于高温环境(34±1)℃、8 h/d,饲喂基础饲粮;热应激+0.18%色氨酸组(HS+0.18%Trp)肉鸡饲养于高温环境(34±1)℃、8 h/d,饲喂基础饲粮+0.18%色氨酸。结果表明:1)与TN组相比,热应激显著降低肉鸡肝脏谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活性、回肠黏膜CAT和超氧化物歧化酶(SOD)活性以及总抗氧化能力(T-AOC)(P<0.05);与HS组相比,HS+0.18%Trp组肝脏CAT活性和T-AOC、空肠黏膜SOD活性和T-AOC以及回肠黏膜SOD活性显著升高(P<0.05)。2)与TN组相比,热应激显著增加肝脏白细胞介素(IL)-1β、IL-6、IL-18和肿瘤坏死因子(TNF-α)的含量(P<0.05);与HS组相比,饲粮添加色氨酸显著降低肝脏IL-1β、IL-18和TNF-α的含量(P<0.05)。3)与TN组相比,热应激显著升高肝脏IL-1β、IL-18,空肠黏膜IL-1β、IL-12A、IL-12B、IL-18、TNF-α和NOD样受体蛋白3(NLRP3),回肠黏膜IL-1β、TNF-α、NLRP3和半胱天冬酶-1(Caspase-1)的mRNA表达量(P<0.05);与HS组相比,饲粮添加色氨酸显著降低肝脏TNF-α、空肠黏膜IL-12A、IL-12B、IL-18、TNF-α和NLRP3,回肠黏膜IL-1β、TNF-α、NLRP3和Caspase-1的mRNA表达量(P<0.05)。综上所述:长期热应激降低肉鸡肝脏和肠道的抗氧化能力,同时诱发肝脏和肠道炎症反应。饲粮添加色氨酸能够缓解热应激引起的肝脏和肠道氧化应激损伤,通过抑制NLRP3炎症小体及下游级联反应,减轻炎症反应。 This experiment was conducted to investigate the regulatory effects of dietary tryptophan(Trp) supplementation on antioxidant capacity,inflammatory response and related signaling pathways in liver and intestine of broilers subjected to heat stress(HS).A total of 180 18-day-old female Arbor Acres broilers were randomly assigned to three treatments with 6 replicates of 10 broilers each.After 3 days of adaptive feeding,temperature control was started at 21 days of age,and the experiment lasted for 21 days.The broilers were either raised under thermoneutral(TN)conditions(23± 1) ℃ or subjected to heat stress((34±1)℃ for 8 h daily.The broilers kept at TN conditions were fed a basal diet,and those exposed to heat stress were fed basal diets supplemented with 0% or 0.18% Trp.The results showed that:1) Compared with TN group,heat stress significantly decreased the activities of glutathione peroxidase(GSH-Px) and catalase(CAT) in liver,and CAT,superoxide dismutase(SOD) activity and total antioxidant capacity(T-AOC) in ileum mucosa of broilers(P<0.05);compared with HS group,CAT activity and T-AOC in liver,SOD activity and T-AOC in jejunum mucosa,and SOD activity in ileum mucosa of broilers in HS+0.18% Trp group were significantly increased(P <0.05).2) Compared with TN group,heat stress significantly increased the contents of interleukin(IL)-1β,IL-6,IL-18 and tumor necrosis factor(TNF-α) in liver(P<0.05);compared with HS group,dietary tryptophan supplementation significantly decreased IL-1β,IL-18 and TNF-α contents in liver(P<0.05).3) Compared with TN group,heat stress significantly increased the mRNA expression levels of IL-1β and IL-18 in liver,IL-1β,IL-12 A,IL-12 B,IL-18,TNF-α and NOD-like receptor protein 3(NLRP3) in jejunum mucosa,and IL-1β,TNF-α,NLRP3 and Caspase-1 in ileum mucosa(P<0.05);compared with HS group,dietary tryptophan supplementation significantly decreased the mRNA expression levels of TNF-α in liver,IL-12 A,IL-12 B,IL-18,TNF-α and NLRP3 in jejunum mucosa,and IL-1β,TNF-α,NLRP3 and Caspase-1 in ileum mucosa(P<0.05).In conclusion,chronic heat stress reduces antioxidant capacity and induces inflammation in liver and intestine of broilers.Dietary tryptophan supplementation alleviates heat stress-induced oxidative damage in liver and intestine,and reduces inflammation by inhibiting NLRP3 inflammasomes and downstream cascade reactions in broilers.
作者 欧阳经鑫 李秋粉 周华 郑俊 郭帅鹏 刘三凤 黎观红 OUYANG Jingxin;LI Qiufen;ZHOU Hua;ZHENG Jun;GUO Shuaipeng;LIU Sanfeng;LI Guanhong(Jiangxi Province Key Laboratory of Animal Nutrition,Jiangxi Agricultural University,Nanchang 330045,China;College of Animal Science and Technology,Jiangxi Agricultural University,Nanchang 330045,China)
出处 《中国兽医学报》 CAS CSCD 北大核心 2022年第6期1256-1262,1269,共8页 Chinese Journal of Veterinary Science
基金 国家自然科学基金资助项目(31860651) 江西省自然科学基金重点资助项目(20181ACB20015) 江西省现代农业家禽产业技术体系资助项目(JXARS-09)。
关键词 色氨酸 热应激 肉鸡 抗氧化能力 炎症细胞因子 tryptophan heat stress broiler antioxidant capacity inflammatory cytokines
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  • 1Weihua Xiao~1 1 University of Science and Technology of China,China.2 Laboratory of Molecular Immunoregulation,NCI-Frederick,Frederick.MD 21702.USA..Advances in NF-κB Signaling Transduction and Transcription[J].Cellular & Molecular Immunology,2004,1(6):425-435. 被引量:21
  • 2Zhou R, Yazdi AS, Menu P, Tschopp J. A role for mitochondria in NLRP3 in- flammasome activation. Nature 2010; 469:221-225.
  • 3Schroder K, Tschopp J. The inflam- masomes. Cell 2010; 140:821-832.
  • 4Martinon F, Mayor A, Tschopp J. The inflammasomes: guardians of the body. Annu Rev lmmuno12009; 27:229-265.
  • 5Jin C, Flavel| RA. Molecular mecha- nism of NLRP3 inflammasome acti- vation. J Clin Immunol 2010; 30:628- 631.
  • 6Dostert C, Guarda G, Romero JF, et al. Malarial hemozoin is a Nalp3 inflam- masome activating danger signal. PLoS One 2009; 4:e6510.
  • 7Li N, Ragheb K, Lawler G, et al. Mito- chondrial complex I inhibitor rotenone induces apoptosis through enhancing mitochondrial reactive oxygen spe- cies production. J Biol Chem 2003; 278:8516-8525.
  • 8Hayashi T, Rizzuto R, Hajnoczky G, Su TP. MAM: more than just a housekeep- er. Trends Cell Bio12009; 19:81-88.
  • 9Saitoh T, Fujita N, Jang MH, et al. Loss of the autophagy protein Atgl6L1 en- hances endotoxin-induced IL-lbeta production. Nature 2008; 456:264- 268.
  • 10Goldman S J, Taylor R, Zhang Y, Jin S. Autophagy and the degradation of mitochondria. Mitochondrion 2010; 10:309-315.

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