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基碳化合物受体 (AhR) 是通过过氧调节在早产婴儿
Xi Yang1,2,3, Xia Wang1,2,3, Wenbin Dong1,2,3
1Division of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
概括
过氧会增加早产婴儿的氧化压力,因为它会影响基碳化合物受体 (AhR). 增加的AhR转位和减少的表达与更高的活性氧物种 (ROS) 和炎症标志物相关.
科学领域:
- 新生儿生理学 新生儿生理学
- 分子生物学分子生物学
- 氧化应激研究研究 氧化应激研究
背景情况:
- 过早出生的婴儿容易受到过氧引起的氧化应激.
- 在这个过程中,基碳化合物受体 (AhR) 的作用尚未完全理解.
研究的目的:
- 为了调查AhR在过氧中介的氧化应激在早产婴儿的参与.
- 为了检查AhR和外围血液单核细胞 (PBMC) 中的活性氧物种 (ROS) 之间的关系.
主要方法:
- 在48小时的氧气暴露后,从早产婴儿收集了PBMC和血.
- 测量了ROS,甲 (MDA) 和单细胞化学吸引蛋白-1 (MCP-1) 的水平.
- 通过免疫光和西式涂抹来评估AhR局部化和表达.
主要成果:
- 增加的氧气度导致ROS,MDA和MCP-1的水平提高.
- 细胞质细胞核转移的AhR增加,而其表达与较高的氧气水平下降.
- ROS,MDA和MCP-1与AhR转位正相关,与AhR表达负相关.
结论:
- 过氧显著影响早产婴儿的AhR调节.
- AhR转位和表达变化与高氧化引起的氧化应激和炎症有关.
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