Zhu Yuping, Yang Pan, Zhai Suzhen, Zhang Chunlin
School of Basic Medicine, Guizhou Medical University, Guiyang, 550025 China.
Food Sci Biotechnol. 2024 Jul 2;33(15):3541-3552. doi: 10.1007/s10068-024-01599-9. eCollection 2024 Dec.
During the aging process, the abilities to maintain homeostasis and resist stress decrease, leading to degenerative changes in tissues and organs. The pathological process of aging is characterized by oxidative stress and cell cycle arrest. alkylamides (ZA) can mitigate hepatic oxidative stress. However, whether ZA can delay aging and the underlying mechanisms are unclear. Herein, ZA were shown to inhibit d-galactose-induced aging in a dose-dependent manner. ZA activated CyclinD1 and CyclinE2 to exert anti-cell cycle arrest effects and activated the Nrf2/HO1 pathway to reduce the accumulated intracellular reactive oxygen species (ROS) and improve antioxidant capacity. Moreover, motor coordination and spontaneous exploration were improved in aging mice administered ZA. Overall, ZA alleviated cell cycle arrest and oxidative stress to delay d-galactose-induced aging.
The online version contains supplementary material available at 10.1007/s10068-024-01599-9.
在衰老过程中，维持体内平衡和抵抗压力的能力下降，导致组织和器官发生退行性变化。衰老的病理过程以氧化应激和细胞周期停滞为特征。烷基酰胺（ZA）可以减轻肝脏氧化应激。然而，ZA是否能延缓衰老及其潜在机制尚不清楚。在此，ZA被证明以剂量依赖的方式抑制d-半乳糖诱导的衰老。ZA激活细胞周期蛋白D1和细胞周期蛋白E2以发挥抗细胞周期停滞作用，并激活Nrf2/HO1途径以减少细胞内活性氧（ROS）的积累并提高抗氧化能力。此外，给予ZA的衰老小鼠的运动协调性和自发探索能力得到改善。总体而言，ZA减轻细胞周期停滞和氧化应激以延缓d-半乳糖诱导的衰老。
在线版本包含可在10.1007/s10068-024-01599-9获取的补充材料。
