尼古丁胺胺单核酸通过NAD+ /SIRT1/p65轴降低了通过NAD+通过SIRT1/p65轴分泌的前炎性细胞因子
Dongyuan Zhang1,2, Zhiqiang Li1,3, Xianbin Meng1,4
1MOE Key Laboratory of Bioinformatics, State Key Laboratory of Complex, Severe, and Rare Diseases, School of Life Sciences, Tsinghua University, Beijing 100084, China.
尼古丁胺胺单核酸 (NMN) 通过阻断衰老相关的分泌表型 (SASP) 作为老化体起作用. 这种抗衰老干预措施通过提高NAD+水平,激活SIRT1和减少衰老细胞的炎症来起作用.
科学领域:
- 细胞衰老 细胞衰老
- 衰老的研究研究.
- 分子生物学分子生物学
背景情况:
- 衰老相关的分泌表型 (SASP) 驱动衰老和慢性疾病.
- SASP是抗衰老干预措施的一个关键目标.
- 形分子是阻断SASP的分子.
研究的目的:
- 为了研究尼古丁胺胺单核酸 (NMN) 作为潜在的老人形.
- 阐明NMN老态活性背后的分子机制.
主要方法:
- 用NMN治疗衰老细胞.
- 测量促炎性细胞因子分泌.
- 评估NAD+水平和SIRT1活动.
- 对p65乙化和活性进行分析.
主要成果:
- NMN显著抑制了老化细胞的前炎性细胞因子分泌.
- 补充NMN可以增加衰老细胞中的NAD+水平.
- NMN激活了SIRT1,导致Lys310.0的p65乙化减少.
- 抑制p65活动导致细胞因子分泌量下降.
结论:
- 通过准NAD+/SIRT1/p65通路,NMN作为一个老态体起作用.
- 通过减轻SASP诱导的炎症,NMN显示出作为一种抗衰老干预的潜力.
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