尼古丁胺通过NAD+依赖脱乙烯化机制预防糖尿病脑炎症
Jeimy Katherine Torres-Méndez1, Julia Niño-Narvión1,2, Patricia Martinez-Santos1
1Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), 08041 Barcelona, Spain.
Nutrients
|July 29, 2023
概括
尼古丁胺胺 (NAM) 补充剂在1型糖尿病小鼠模型中降低了大脑炎症和微质激活. 这种神经保护作用与增加的NAD+水平和NAD+依赖的脱乙化机制有关.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
背景情况:
- 1型糖尿病 (T1D) 与神经系统并发症的风险增加有关.
- 大脑炎症和微质激活是糖尿病脑病变的关键病理特征.
- 尼古丁胺 (NAM) 是一种维生素B3的形式,是NAD+的前体,具有潜在的抗炎性质.
研究的目的:
- 在1型糖尿病小鼠模型中研究尼古丁胺胺 (NAM) 补充剂在减轻大脑炎症和微质激活方面的疗效.
- 探索潜在的分子机制,包括NAD+代谢和NFκB信号通路.
主要方法:
- 在C57BL/6J雄性小鼠中,使用链毒素 (STZ) 诱导了1型糖尿病.
- 糖尿病小鼠接受低剂量 (LD) 或高剂量 (HD) NAM补充剂25天.
- 对大脑组织进行了NAD+含量,炎症标记物 (TNFα),微质激活标记物 (IBA-1,BDKRB1) 和NFκB信号传递 (p65乙化) 的分析.
主要成果:
- 在糖尿病小鼠中,NAM补充剂显著增加了大脑的NAD+水平.
- NAM治疗显著降低了炎症标志物和微质激活.
- NFκB (p65) 信号减轻,核p65减少和p65乙化减少,与NAD+含量相反相关.
结论:
- 在T1D小鼠模型中,食NAM补充剂有效地预防了大脑炎症和微质激活.
- 神经保护作用是由NAD+依赖的脱甲基化机制调解的,这表明增强了Sirtuin信号传递.
- NAM显示了在1型糖尿病中控制神经炎症的治疗潜力.
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