3'-酸乳糖通过抑制超氧化物介导的ERK1/2/STAT1激活和HMGB1/RAGE轴来保护LPS诱导的内皮功能障碍
Dung Van Nguyen1, Yujin Jin1, Thuy Le Lam Nguyen1
1College of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon 34134, South Korea.
Life sciences
|January 8, 2024
概括
3'-Sialyllactose (3'-SL) 通过降低氧化应激和抑制关键炎症通路,防止内皮功能障碍. 这表明3'-SL可能是动脉样硬化的新疗法.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞生物学 内皮细胞生物学
- 分子医学是分子医学.
背景情况:
- 内皮膜的超透性是动脉样硬化发展的一个关键因素.
- 在人乳中丰富的3-酸乳糖 (3-SL) 在调节内皮功能障碍方面显示出潜力.
研究的目的:
- 在体外和体内研究3 -SL对脂聚糖 (LPS) 诱导的内皮功能障碍的保护作用.
- 阐明3 -SL作用的潜在分子机制.
主要方法:
- 在牛大动脉内皮细胞 (BAEC) 和小鼠中建立了LPS诱导的内皮功能障碍模型.
- 使用西式涂抹,qRT-PCR,免疫光和面部染色来分析机制.
- 使用光探针量化超氧化物生产.
主要成果:
- 3 -SL治疗通过抑制ERK1/2激活缓解了LPS诱导的细胞活力下降.
- 3 -SL减少了活性氧物种 (ROS) 的积累,抑制了STAT1酸化和下游炎症基因 (VCAM-1,TNF-α,IL-1β,MCP-1).
- 3 -SL抑制了HMGB1/RAGE轴,防止了VE-cadherin的分解和内皮单层的破坏.
结论:
- 3 -SL通过抑制超氧化物介导的ERK1/2/STAT1激活和HMGB1/RAGE轴来抑制LPS诱导的内皮透气性.
- 3 -SL显示出作为预防动脉样硬化进展的治疗剂的潜力.
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