Abstract
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. Zanthoxylum 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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-024-01599-9.