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通过NAD+/SIRT1通路,NMN可以保护与青相关的AKI
Zhaozhi Wen1,2, Jiazeng Wang1, Yihang Yang1
1School of Life Sciences, Nantong Laboratory of Development and Diseases, Nantong University, Nantong, Jiangsu, China.
Frontiers in immunology
|February 20, 2026
概括
尼古丁胺胺氨基二核酸 (NAD+) 前体β-尼古丁胺胺单核酸 (NMN) 在预防西斯普拉丁相关急性损伤 (CIS-AKI) 中显示出有前途. 通过激活NAD+-SIRT1通路,NMN可以减少损伤,炎症和氧化应激.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 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:
- 急性损伤 (AKI) 是一个重大的临床挑战,西斯普拉丁化疗经常导致损伤 (CIS-AKI).
- 尼古丁胺胺氨基二核酸 (NAD+) 对于细胞代谢至关重要,其前体β-尼古丁胺胺 mononucleotide (NMN) 在其他疾病中已经显示出治疗潜力.
- 在此之前,NMN在缓解CIS-AKI方面的具体作用尚不清楚.
研究的目的:
- 调查NMN对西斯普拉丁诱导的AKI (CIS-AKI) 的保护作用.
- 在CIS-AKI模型中阐明NMN作用的基本机制.
主要方法:
- 使用雄性小鼠和HK-2细胞作为CIS-AKI的体内和体外模型.
- 管理NMN以评估其对功能,损伤标志物,炎症和氧化应激的影响.
- 采用大量RNA测序来分析脏组织的变化,并测量NAD+水平和SIRT1表达.
主要成果:
- 服用NMN显著改善了功能,降低了肌和血尿素 (BUN) 水平.
- NMN减弱了损伤标志物 (NGAL,KIM-1),抑制了炎症 (IL-6,IL-18),并减少了免疫细胞的透.
- 在体外,NMN降低了在西斯治疗细胞中的活性氧物种 (ROS) 和乳酸脱酶 (LDH) 的释放.
- NMN提高了中的NAD+水平,增加了SIRT1的表达,表明NAD+-SIRT1通路的激活.
结论:
- NMN显示出显著的脏保护作用,防止西斯普拉丁诱导的AKI.
- NMN通过增强NAD+-SIRT1通路而起作用,从而减轻氧化应激和炎症.
- NMN为预防和治疗CIS-AKI提供了潜在的治疗策略.
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