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奎尔素预防保护脏通过调节氨酸- ангиотензин-阿尔多斯轴在急性低氧性压力下保护脏
Vaishnavi Rathi1, Sarada S K Sagi2, Amit Kumar Yadav3
1Defence Institute of Physiology and Allied Sciences, DRDO, Lucknow Road, Timarpur, New Delhi, 110054, India.
Scientific reports
|March 31, 2024
概括
奎尔西预防有效地通过减少氧化应激和炎症来减轻低性缺氧效应. 它调节了Renin-Angiotensin-Aldosterone系统 (RAAS) 途径,可能通过ACE 2相互作用,改善了适应低氧条件的适应性.
科学领域:
- 身体生理学 身体生理学
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 低性缺氧会引发氧化应激,并破坏雷宁-氨-阿尔多斯系统 (RAAS).
- 了解这些影响对于改善人类适应高海拔环境至关重要.
研究的目的:
- 评估催性缺氧对RAAS通路的影响.
- 评估奎尔塞丁在缓解缺氧引起的异常方面的疗效.
主要方法:
- 雄性斯普拉格-道利大鼠被暴露在模拟的低氧 (25,000英尺) 中.
- 奎尔赛丁和乙胺被口服作为预防药物.
- 分析了等离子体中的生物化学参数 (renin, aldosterone, ACE 2,氧化应激标志物) 和蛋白质表达 (HIF-1α, NFκB).
- 表面等离子体共振 (SPR) 用于研究氨酸-ACE2结合.
主要成果:
- 低性缺氧增加了氧化应激 (ROS,MDA) 和抑制了抗氧化剂 (GPx,Catalase).
- 奎尔素显著降低了氧化应激,增强了抗氧化活性.
- 奎尔素有效调节了缺氧引起的和ACE2的变化,并降低了炎症标志物 (HIF-1α,NFκB,IL-18,endothelin-1).
- SPR证实了奎尔塞丁与ACE2之间的直接结合.
结论:
- 奎尔赛丁预防证明了在抵消催性缺氧诱导的氧化应激和炎症方面显著的有效性.
- 奎尔塞丁调节RAAS通路,可能通过与ACE2的相互作用,增强适应性,以hypobaric缺氧条件.
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