College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, China.
Zhongkai University of Agriculture and Engineering, Guangzhou, 510225, China.
Environ Sci Pollut Res Int. 2018 Jul;25(21):21011-21023. doi: 10.1007/s11356-018-2142-8. Epub 2018 May 15.
The aim of this study was to investigate the role of heat shock protein 70 (Hsp70) in oxidative stress and inflammatory damage in the spleen of quails which were induced by cold stress. One hundred ninety-two 15-day-old male quails were randomly divided into 12 groups and kept at 12 ± 1 °C to examine acute and chronic cold stress. We first detected the changes in activities of antioxidant enzymes in the spleen tissue under acute and chronic cold stress. The activities of glutathione peroxidase (GSH-Px) fluctuated in acute cold stress groups, while they were significantly decreased (p < 0.05) after chronic cold stress. The activities of superoxide dismutase (SOD), inducible nitric oxide synthase (iNOS), and nitric oxide (NO) content were decreased significantly (p < 0.05) in both of the acute and chronic cold stress groups. Malondialdehyde (MDA) content was significantly increased (p < 0.05) under cold stress except the 0.5 h group of acute cold stress. Besides, histopathological analysis showed that quail's spleen tissue was inflammatory injured seriously in both the acute and chronic cold stress groups. Additionally, the inflammatory factors (cyclooxygenase-2 (COX-2), prostaglandin E synthase (PTGES), iNOS, nuclear factor-kappa B (NF-κB), and tumor necrosis factor-a (TNF-α)) and Hsp70 mRNA levels were increased in both of the acute and chronic cold stress groups compared with the control groups. These results suggest that oxidative stress and inflammatory injury could be induced by cold stress in spleen tissues of quails. Furthermore, the increased expression of Hsp70 may play a role in protecting the spleen against oxidative stress and inflammatory damage caused by cold stress.
本研究旨在探讨热休克蛋白 70（Hsp70）在冷应激诱导的鹌鹑脾脏氧化应激和炎症损伤中的作用。将 192 只 15 日龄雄性鹌鹑随机分为 12 组，在 12±1°C 下饲养以检测急性和慢性冷应激。我们首先检测了急性和慢性冷应激下脾脏组织中抗氧化酶活性的变化。急性冷应激组谷胱甘肽过氧化物酶（GSH-Px）活性波动，而慢性冷应激后则显著降低（p<0.05）。超氧化物歧化酶（SOD）、诱导型一氧化氮合酶（iNOS）和一氧化氮（NO）含量活性在急性和慢性冷应激组均显著降低（p<0.05）。急性冷应激组除 0.5 h 组外，丙二醛（MDA）含量均显著升高（p<0.05）。此外，组织病理学分析表明，急性和慢性冷应激组鹌鹑脾脏组织均发生严重炎症损伤。另外，急性和慢性冷应激组炎症因子（环氧化酶-2（COX-2）、前列腺素 E 合酶（PTGES）、iNOS、核因子-κB（NF-κB）和肿瘤坏死因子-α（TNF-α））和 Hsp70 mRNA 水平均高于对照组。这些结果表明，冷应激可导致鹌鹑脾脏组织发生氧化应激和炎症损伤。此外，Hsp70 的表达增加可能在保护脾脏免受冷应激引起的氧化应激和炎症损伤中发挥作用。
