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首页> 外文期刊>Environmental Science and Pollution Research >Protective effects of dietary mannan oligosaccharide on heat stress-induced hepatic damage in broilers
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Protective effects of dietary mannan oligosaccharide on heat stress-induced hepatic damage in broilers

机译:膳食甘露糖糖对肉鸡热应激诱导的肝损伤的保护作用

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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 degrees 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 alpha (TNF-alpha) in the serum and liver, interleukin-1 beta (IL-1 beta) in the liver, and mRNA abundances of HSP70, TLR4, MyD88, TNF-alpha, and IL-1 beta in the liver of broilers. Serum TNF-alpha content and mRNA abundances of hepatic TLR4 and TNF-alpha 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.
机译:热应激是肉鸡生产的一个主要问题,这可能会损坏肉鸡的肝脏。本研究对肉鸡热应激诱导的肝损伤的研究甘露寡糖(MOS)的保护作用。共144日龄雄性雏鸡被分为三个处理组。正常环境温度下饲养肉仔鸡,饲喂基础饮食(对照组),和热胁迫下肉鸡(32-33摄氏度每天8小时)给予无MOS(热应激组),补充基础饮食或用1克/公斤MOS(MOS组)42天。与对照组,热应力降低肝脏重量相比,而增加的天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)血清中的活动。它也减少谷胱甘肽过氧化物酶(谷胱甘肽过氧化物酶)在肝脏中的血清和肝,GSH含量,和超氧化物歧化酶(SOD)活性的活性,但血清和肝脏中增加丙二醛(MDA)的浓度。膳食MOS在热应激肉鸡降低血清ALT活性。 MOS夹杂也降低血清MDA含量,但升高的肝GSH-Px和SOD活性,与MDA含量和GSH-Px活性仍然与对照组不同,SOD活性相似于对照组。热应力的血清和肝脏中增加的肿瘤坏死因子α(TNF-α)的浓度,在肝脏中白细胞介素-1β(IL-1β),和mRNA丰度HSP70,TLR4,MyD88的,TNF-α和IL的-1公测肉鸡的肝脏。血清TNF-α含量和肝TLR4 mRNA的丰度和TNF-α在MOS组较热应激组低,而这些指标均仍比对照组更高。我们的研究结果表明,膳食MOS通过氧化应激和炎症减轻改善在热应激肉鸡肝损伤。

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