普雷瓦基诺A抑制了AMPK的 ангиотензинII诱导的内皮透气功能障碍激活
Si Chen1, Jun-di Xie2, Meng-Ting Xie2
1Department of Traditional Chinese Medicine, Institute of Integration of Traditional and Western Medicine of Guangzhou Medical University, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510260, PR China; School of Chinese medicine, Hong Kong Baptist University (HKBU), Kowloon Tong, Kowloon, Hong Kong, PR China.
概括
普雷瓦基A (PA) 激活了腺5'-单酸盐 (AMP) 激活的蛋白激酶 (AMPK),以防止内皮功能障碍和高血压. 这项研究调查了PAPA.
科学领域:
- 心血管药理学心血管药理学
- 内皮细胞生物学 内皮细胞生物学
- 高血压的分子机制 高血压的分子机制
背景情况:
- 内皮功能障碍 (ED) 涉及氧化 (NO) 生物可用性降低,血管收缩和炎症,导致心血管疾病.
- 氨酸5-单酸盐 (AMP) 激活蛋白激酶 (AMPK) 在心血管发育中起着至关重要的作用.
- 众所周知,Przewaquinone A (PA) 是Salvia przewalskii的提取物,可以抑制血管收缩.
研究的目的:
- 在体外和体内研究普雷瓦基A (PA) 对内皮功能障碍 (ED) 的保护作用.
- 阐明PA改善ED的潜在分子机制.
主要方法:
- 在体外:人类静脉内皮细胞 (HUVECs) 暴露于血管素II (AngII) 以建模ED.
- 在体内:输入AngII的高血压小鼠模型;测量包括血压,血管度,NO和内甲蛋白-1 (ET-1) 水平.
- 分子技术:西部涂抹,ELISA,免疫组织化学,分子对接,分子动力学和表面等离子体共振成像 (SPRi) 以评估AMPK激活和PA-AMPK相互作用.
主要成果:
- PA抑制了AngII诱导的血管收缩和血管粘附,剂量取决于激活AMPK信号.
- 它降低了血压,在高血压小鼠中增强了血管扩张,并促进了AMPK激活.
- 分子模拟和SPRi证实了PA对AMPK的直接向;AMPK抑制部分逆转了PA的保护作用.
结论:
- 普雷瓦基A (PA) 直接激活AMPK信号传递.
- 帕显示出对内皮功能障碍和高血压的显著保护作用.
- 这些发现突出了PA作为涉及ED的心血管疾病的潜在治疗剂.
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