银化物Rg1通过TXNIP/NLRP3路径调节的线粒细胞衰变改善缺氧诱导的肺血管内皮功能障碍
Ru Zhang1, Meili Lu1, Chenyang Ran1
1The Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Jinzhou Medical University, Jinzhou, China.
Journal of ginseng research
|January 28, 2025
概括
银化物Rg1 (Rg1) 通过调节TXNIP/NLRP3通路,减少氧化应激,炎症和线粒细胞衰变,改善肺动脉高血压中的肺血管内皮功能障碍.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 肺动脉高血压 (PAH) 涉及血管内皮功能障碍 (VED).
- 银化物Rg1 (Rg1) 显示出改善PAH的潜力,但其在缺氧诱导的VED中的机制尚未完全理解.
研究的目的:
- 阐明Rg1在低氧诱导的PAH中影响肺VED的机制.
- 为了研究Rg1在氧化应激,炎症,线粒和TXNIP/NLRP3通路中的作用.
主要方法:
- 已确定的缺氧诱导的PAH小鼠 (SuHx模型) 和细胞模型.
- 利用了网络药理学和分子对接.
- 研究了Rg1对VED,氧化应激,炎症,线粒和TXNIP/NLRP3表达的作用.
主要成果:
- 低氧诱导VED,氧化应激,炎症和线粒细胞衰变,与TXNIP和NLRP3.3升高有关.
- Rg1改善了内皮依赖的血管扩张,增加了氧化 (NO) 和内皮NO合成酶 (eNOS).
- 通过减少TXNIP/NLRP3.3,Rg1,TXNIP抑制剂 (SRI37330),NLRP3抑制剂 (MCC950) 和线粒细胞衰变抑制剂 (Liensinine) 减弱了VED标记物. 线粒细胞衰变的激动剂破坏了Rg1的保护作用.
结论:
- Rg1可以改善缺氧引起的肺部VED.
- 保护机制涉及调节TXNIP/NLRP3通路,从而调节氧化应激,炎症和线粒细胞衰变.
更多相关视频
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
339
07:14A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
14.2K
相关概念视频
01:24Regulation of Angiogenesis and Blood Supply
2.5K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.5K
01:28Nitric Oxide Signaling Pathway
4.9K
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
4.9K