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阿斯特拉加索酸IV通过Akt/Nrf2通路保护LO2细胞免受辐射诱导的旁观者效应引起的氧化损伤

Danting Wan¹, Zihao Zhu¹, Jie Zhou¹

¹Department of Preventive Medicine, School of Public Health, Hengyang Medical School, University of South China, 28 West Changsheng Road, Hengyang, 421001, China.

Toxicology research

|September 4, 2023

概括

甲酸IV (ASIV) 通过减少氧化损伤,保护细胞免受辐射诱导的旁观者效应 (RIBE). ASIV激活了Akt/Nrf2通路,减轻了LO2细胞中RIBE诱导的损害.

科学领域:

细胞和分子生物学细胞和分子生物学
辐射生物学辐射生物学
氧化压力研究研究氧化压力研究

背景情况:

对于各种疾病而言,已知黄IV (ASIV) 的保护作用.
它在减轻辐射诱导旁观者效应 (RIBE) 中的作用仍在调查中.

研究的目的:

研究ASIV对LO2细胞中RIBE诱导的氧化损伤的保护机制.
阐明Akt/Nrf2信号通路在ASIV的保护作用中的参与.

主要方法:

一个辐射诱导的旁观者效应 (RIBE) 模型是使用从被照射的HepG2细胞转移到LO2细胞的条件介质建立的.
评估了ASIV对细胞增殖,线粒体膜潜力,亡和氧化应激标志物的影响.
使用西斑和免疫光分析来评估蛋白质表达和通路激活,包括Akt/Nrf2通路.

主要成果:

ASIV显著改善了LO2细胞增殖,线粒体功能,并减少了亡.
通过调节活性氧物种,抗氧化酶和脂质过氧化,ASIV治疗恢复了氧化应激平衡.
ASIV促进了Nrf2的核转移,激活了下游目标,并证明了对RIBE的保护作用,而RIBE被Akt路径抑制剂废除.

结论:

甲酸IV (ASIV) 能保护LO2细胞免受辐射诱导的旁观者影响 (RIBE).
保护机制包括Akt/Nrf2信号通路的激活,从而减少氧化损伤.

关键词:

在 Akt/Nrf2 路径上.阿斯特拉加洛西德IV 氧化损伤是因为氧化损伤.辐射诱导的旁观者效应

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