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关于保护性氧化作用的米R-221是由改性Codonopsis pilosula多糖化合物诱导的

Tao Qin¹, Mengke Sun¹, Yongyuan Huang²

¹Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health in Fujian Province, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China.

International journal of biological macromolecules

|August 18, 2024

概括

微RNA-221 (miR-221) 保护免受sCPPS5.1诱导的氧化应激. 这种保护由Keap1-Nrf2-ARE信号通路介导,突出显示miR-2212.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

氧化应激与许多疾病有关.
已知微RNA-221 (miR-221) 能够调节氧化应激.
在sCPPS5引起的氧化应激中,miR-221的精确机制尚未完全理解.

研究的目的:

为了阐明miR-221对sCPPS5诱导的氧化应激的保护作用.
调查潜在的分子机制,特别是Keap1-Nrf2-ARE信号通路.

主要方法:

评估的氧化应激标志物:SOD,CAT,MDA,LDH,MMP,caspase-3活性,以及亡.
利用实时PCR和西斑来分析Keap1-Nrf2-ARE路径组件.
使用小鼠模型在体内评估效应.

主要成果:

sCPPS5治疗,特别是miR-221模仿剂,增强了SOD和CAT的表达.
启动了Keap1-Nrf2-ARE信号通路,导致MDA,MMP,caspase-3活性,亡和LDH释放的减少.
在体内研究证实了sCPPS5增强抗氧化酶和关键信号蛋白的能力.

结论:

miR-221可以保护sCPPS5引起的氧化应激.
这种保护作用可能是通过调节巨细胞中的Keap1-Nrf2-ARE信号通路来调节的.
研究结果表明,miR-221在管理与氧化压力相关的疾病方面具有潜在的治疗作用.

关键词:

凯普1-Nrf2信号通道 Codonopsis pilosula 是一种多糖化合物.在 miR-22121 系统中,

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