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曼南结合性莱克通过NAD+/Sirt1通路抑制氧化应激诱导的衰老

Yiming Lei¹, Jie Meng¹, Haiqiang Shi²

¹Xinxiang Key Laboratory of Immunoregulation and Molecular Diagnostics, School of Medical Technology, Xinxiang Medical University, Xinxiang 453003, China.

International immunopharmacology

|June 21, 2024

概括

曼南结合性莱克 (MBL) 通过激活NAD+/Sirt1通路来对抗氧化应激和过早衰老. 这项研究表明MBL.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

氧化应激加速细胞和生物的衰老.
曼南结合性莱克 (MBL) 对先天免疫,抗炎症和抗氧化至关重要,影响健康和寿命.
MBL在减轻氧化应激诱导衰老中的作用需要进一步研究.

研究的目的:

评估MBL在氧化应激引起的过早衰老中的作用.
探索MBL在衰老中的作用的潜在分子机制.
在小鼠模型和细胞培养中研究MBL的影响.

主要方法:

在C57BL/6小鼠中建立D-银糖诱导的氧化过早衰老模型.
在小鼠胚胎纤维细胞中使用过氧化 (H2O2) 诱导的氧化衰老模型 (NIH / 3T3).
评估MBL对衰老标记,氧化应激,DNA损伤,线粒体功能以及NAD+/Sirt1通路的影响.

主要成果:

缺乏MBL的小鼠表现出加速衰老的表型,认知缺陷,肝损伤,衰老标志物 (p53,p21,SA-β-Gal) 和炎症 (IL-1β,IL-6) 的增加.
在NIH/3T3细胞中的MBL干预逆转了氧化应激诱导的衰老,减少ROS,DNA损伤和G1停止.
MBL激活了NAD+/Sirt1通路,上调了NAMPT,并抑制了p38酸化,抵消了氧化应激效应.

结论:

MBL有效地抑制了氧化应激诱导的过早衰老.
MBL的机制包括激活NAD+/Sirt1通路.
这些发现表明MBL是延缓氧化衰老的潜在治疗标.

关键词:

曼南结合性学菌素是一种曼南结合性学菌素.尼古丁胺胺腺因二核酸是什么氧化应激是一种氧化应激.衰老是一种衰老.在 Sirtuin 11 里面,我们可以找到 Sirtuin 11.

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