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增强NAD增加了Apoe淘汰赛小鼠的动脉样硬化斑块和炎症

Yu-Jen Wang¹, Daniel S Gaul², Era Gorica¹

¹Center for Translational and Experimental Cardiology (CTEC), Department of Cardiology, University Hospital Zurich and University of Zurich, Zurich, Switzerland; Department of Cardiology, University Heart Center Zurich, University Hospital Zurich, Zurich, Switzerland.

Atherosclerosis

|April 11, 2025

概括

高剂量的尼古丁胺胺 рибоoside (NR) 补充剂在小鼠中恶化了动脉样硬化和炎症. 这表明,在患有心血管风险的患者中,应谨慎使用NAD+增强剂.

科学领域:

生物化学生物化学
心血管研究研究心血管研究
代谢健康代谢健康

背景情况:

尼古丁胺胺二核酸 (NAD+) 对于Sirtuin活性至关重要,这与热量限制的好处有关.
像尼古丁胺基核酸 (NR) 这样的NAD+前体被用于抗衰老和代谢健康,但它们对心血管的影响尚不清楚.
赛尔图因,PARP1和CD38竞争NAD+,影响其代谢命运.

研究的目的:

为了研究尼古丁胺 рибоoside (NR) 补充剂的潜在体外保护作用.
确定NR如何影响NAD+代谢和动脉样硬化背景下的炎症标志物.

主要方法:

在12周的时间里,Apolipoprotein E淘汰赛小鼠被食高胆固醇饮食,并补充了不同剂量的NR.
巨细胞 (RAW264.7和骨髓衍生) 被氧化LDL和NR刺激.
测量包括大动脉斑块病变,血炎性细胞因子,脂质概况和NAD+代谢物.

主要成果:

高剂量的NR (NR++) 增加了大动脉斑块病变和TNFα,IL-6和LDL胆固醇的血水平.
肝脏和血NAD+水平没有变化,但代谢物4PY增加.
补充NR导致巨细胞和肝脏中的CD38表达增加,SIRT1减少和PARP1活性增加.

结论:

高剂量的NR补充剂在小鼠中加剧了动脉样硬化和全身炎症,与预期的益处相反.
这些发现表明,NAD+代谢的转移远离sirtuins,转向CD38和PARP1通路.
建议在考虑对患有动脉样硬化的个体进行NR等NAD+提升策略时谨慎.

关键词:

动脉样硬化是一种动脉样硬化.CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 肝脏肝脏肝脏肝脏巨细胞是一个巨细胞.尼古丁胺胺氨基二核酸 (NAD(+))尼古丁胺胺里化物 (NR)

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