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寒冷刺激会通过调节Nrf2/HO-1和NF-κB通路在肉心脏中引起氧化应激,炎症反应和亡
Haidong Wei1, Tingting Li1, Yong Zhang1
1College of Life Science, Northeast Agricultural University, 150030, Harbin, China.
Journal of thermal biology
|July 18, 2023
概括
严重的寒冷压力 (9°C低于正常) 通过Nrf2/HO-1通路增加氧化压力,炎症和亡,损害肉心脏. 温和的寒冷压力 (3°C低于正常) 提高了心脏的适应能力,没有不良影响.
科学领域:
- 动物科学动物科学
- 环境生理学环境生理学
- 心血管研究研究心血管研究
背景情况:
- 寒冷压力是一个重要的环境挑战,影响家禽的健康和生产力.
- 了解心脏对寒冷的反应对于改善肉福利和表现至关重要.
研究的目的:
- 为了研究不同程度的冷刺激对肉心脏组织的影响.
- 阐明导致寒冷引起的心脏损伤的分子机制,重点关注氧化应激,炎症和亡.
主要方法:
- 300只一天大的母肉被分为对照,轻度 (3°C低于正常) 和严重 (9°C低于正常) 寒冷刺激组.
- 在15-35日之间,每天进行5小时的冷刺激.
- 在多个时间点分析了心脏组织的氧化应激标记,炎症指标,亡相关的蛋白质和基因表达.
主要成果:
- 严重的冷刺激 (低于正常的9°C) 导致显著的心肌炎症,氧化应激增加 (MDA和H2O2升高,抗氧化酶活性降低) 和亡增强 (Bax,caspase-3/9增加;Bcl-2减少).
- 在严重感冒组中,基因表达分析显示了抗氧化途径 (Nrf2,HO-1,SOD,CAT,GPx) 的下调和炎症标志物 (NF-κBp65,COX-2,TNF-α,IL-1β) 的上调.
- 温和的冷刺激 (3°C低于正常) 对心脏参数没有造成显著的有害影响,这表明适应能力有所改善.
结论:
- 严重的寒冷压力导致 brojlers 显著的心脏病理,主要是通过氧化压力,炎症和亡,由 Nrf2 / HO-1 信号通路介导.
- 温和的寒冷刺激可能会增强肉心脏的弹性和适应寒冷环境的能力.
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