来自Sanguisorba officinalis L.的butanol提取物的血管扩张作用及其机制
Hangyu Jin1, Jiaze Li2, Shuyuan Wang3
1Clinical Medicine, College of Medicine, Yanbian University, Yanji 133002, China.
Plants (Basel, Switzerland)
|April 12, 2025
概括
迪尤 (BSO) 的醇提取物通过激活内皮细胞中的PI3K-Akt-eNOS-NO通路和光滑肌细胞中的NO-sGC-cGMP-K+通道通路来促进血管放松. 这种提取物还影响信号传递,并降低大鼠的血压.
科学领域:
- 药理学 药理学是指药理学的学科.
- 心血管研究研究心血管研究
- 自然产品化学 自然产品化学
背景情况:
- Sanguisorba officinalis L. (Diyu) 根提取物表现出各种药理性质.
- 了解Diyu的血管放松机制对于其治疗潜力至关重要.
研究的目的:
- 为了研究Diyu (BSO) 的butanol提取物的血管松作用的机制.
- 阐明参与BSO诱导血管扩张的信号通路.
主要方法:
- 使用初级培养的人类静脉内皮细胞 (HUVEC) 来评估氧化 (NO) 生产和信号通路激活.
- 隔离的老鼠胸前大动脉环被用于评估对BSO的反应中的血管松效应.
- 使用特定途径抑制剂 (L-NAME,沃特曼宁,ODQ,TEA) 和调节剂进行了抑制研究.
- 在体内研究评估了BSO对大鼠缩血压和心率的影响.
主要成果:
- 通过PI3K-Akt-eNOS通路,BSO通过HUVEC显著增加了氧化 (NO) 的产生.
- 在老鼠大动脉环中,BSO诱导了依赖于度的血管松,依赖于内皮.
- 由BSO诱导的血管扩张涉及NO-sGC-cGMP通路和血管光滑肌中的K+通道激活.
- BSO调节的细胞内水平和存储运行的入量 (SOCE).
- 在老鼠中,BSO降低了缩血压和心率.
结论:
- 通过一个复杂的内皮依赖机制,BSO诱导血管松.
- 涉及的关键通路包括内皮细胞中的PI3K-Akt-eNOS-NO和光滑肌细胞中的NO-sGC-cGMP-K+通道.
- 调节信号和SOCE有助于BSO的血管效应.
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