College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, People's Republic of China.
Environ Sci Pollut Res Int. 2020 Aug;27(23):29000-29008. doi: 10.1007/s11356-020-09212-2. Epub 2020 May 18.
Heat stress is a major concern in broiler's production, which can damage liver of broilers. This study investigated the protective effects of mannan oligosaccharide (MOS) on heat stress-induced hepatic injury in broilers. A total of 144 day-old male chicks were allocated into three treatment groups. Broilers raised under normal ambient temperature were fed a basal diet (control group), and broilers under heat stress (32-33 °C for 8 h daily) were given the basal diet supplemented without MOS (heat stress group) or with 1 g/kg MOS (MOS group) for 42 days. Compared with the control group, heat stress reduced liver weight, whereas increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in the serum. It also reduced glutathione peroxidase (GSH-Px) activity in the serum and liver, GSH content, and superoxide dismutase (SOD) activity in the liver, but increased malondialdehyde (MDA) concentration in the serum and liver. Dietary MOS decreased serum ALT activity in heat-stressed broilers. MOS inclusion also decreased serum MDA content, but elevated hepatic GSH-Px and SOD activities, with MDA content and GSH-Px activity still being different from the control group, and SOD activity being similar to the control group. Heat stress increased concentrations of tumor necrosis factor α (TNF-α) in the serum and liver, interleukin-1β (IL-1β) in the liver, and mRNA abundances of HSP70, TLR4, MyD88, TNF-α, and IL-1β in the liver of broilers. Serum TNF-α content and mRNA abundances of hepatic TLR4 and TNF-α in MOS group were lower than the heat stress group, whereas these indexes were still higher than the control group. Our results indicated that dietary MOS ameliorated hepatic damage in heat-stressed broilers through alleviation of oxidative stress and inflammation.
热应激是肉鸡生产中的一个主要关注点,它会损害肉鸡的肝脏。本研究探讨了甘露寡糖(MOS)对热应激诱导肉鸡肝损伤的保护作用。将 144 只 1 日龄雄性小鸡分为三组。在正常环境温度下饲养的肉鸡喂食基础日粮(对照组),而在热应激(每天 32-33°C 持续 8 小时)下饲养的肉鸡喂食基础日粮,不添加 MOS(热应激组)或添加 1g/kg MOS(MOS 组),共 42 天。与对照组相比,热应激降低了肉鸡的肝脏重量,而增加了血清中天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活性。它还降低了血清和肝脏中的谷胱甘肽过氧化物酶(GSH-Px)活性、肝脏中的谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活性,而增加了血清和肝脏中的丙二醛(MDA)浓度。日粮 MOS 降低了热应激肉鸡的血清 ALT 活性。MOS 还降低了血清 MDA 含量,但提高了肝脏中的 GSH-Px 和 SOD 活性,MDA 含量和 GSH-Px 活性仍与对照组不同,SOD 活性与对照组相似。热应激增加了血清和肝脏中肿瘤坏死因子-α(TNF-α)、肝脏中白细胞介素-1β(IL-1β)以及肝脏中 HSP70、TLR4、MyD88、TNF-α和 IL-1β 的 mRNA 丰度。MOS 组血清 TNF-α含量和肝脏 TLR4 和 TNF-α 的 mRNA 丰度低于热应激组,但仍高于对照组。我们的结果表明,日粮 MOS 通过缓解氧化应激和炎症改善了热应激肉鸡的肝脏损伤。