AMPK通过控制氧化应激负面调节RANKL诱导的骨质细胞分化,通过控制氧化应激
Miori Tanaka1, Hirofumi Inoue2, Nobuyuki Takahashi2
1Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo, 156-8502, Japan; The Nippon Foundation Human Milk Bank, 17-10 Nihonbashi-koamicho, Chuo-ku, Tokyo, 103-0016, Japan.
Free radical biology & medicine
|June 3, 2023
概括
AMP激活蛋白激酶 (AMPK) 通过抑制通过抗氧化途径的骨质细胞分化来调节骨代谢. 用植物化学物质激活AMPK可以通过减少骨再吸收来治疗骨疾病.
科学领域:
- 生物化学 生化学
- 细胞生物学 细胞生物学
- 代谢过程中的代谢.
背景情况:
- AMP激活蛋白激酶 (AMPK) 是一个关键的细胞能量传感器,参与了代谢调节.
- AMPK缺乏与骨质细胞数量增加和骨质量减少有关,但根本机制尚未完全理解.
研究的目的:
- 阐明AMPK与骨质细胞分化之间的机制联系.
- 调查AMPK在植物化学品骨保护作用中的作用.
主要方法:
- 利用siRNA在经历骨质细胞分化的细胞中击败AMPK表达.
- 评估了AMPK淘汰对骨质细胞形成,基因表达和信号通路 (MAPK,NF-κB) 的影响.
- 评估了抗氧化剂治疗 (N-乙-l-氨酸) 和植物化学物质 (hesperetin,酸,白醇,黄素) 对骨质细胞分化的影响.
主要成果:
- 抑制AMPK促进了RANKL诱导的骨质细胞分化和MAPK和NF-κB信号的激活.
- 缺乏AMPK会损害血红氧酶-1和Nrf2的合成,这是抗氧化剂防御系统的关键组成部分.
- 抗氧化剂治疗和激活AMPK的植物化学物质抑制了骨质细胞分化和相关的信号通路.
结论:
- 通过增强抗氧化剂防御系统和管理氧化应激,AMPK抑制骨质细胞分化.
- 通过饮食中的植物化学物质激活AMPK,为具有过度骨再吸收特征的骨疾病提供了潜在的治疗策略.
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