Su Huijuan, Li Yutao, Wan Jiayi, Lin Jieyu, Wang Jiayao, Fan Rui, Liu Dingming, Wei Jing, Xin Hongbo, Hua Yuejin, Li Shengjie
School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.
National Engineering Research Center for Bioengineering Drugs and the Technologies, Jiangxi Province Key Laboratory of Bioengineering Drugs, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Xuefu Avenue 1299, Honggutan New District, Nanchang, 330031, Jiangxi Province, China.
Mol Neurobiol. 2025 Jul 19. doi: 10.1007/s12035-025-05215-7.
Deinoxanthin (DX), a special hydroxylated tetraterpenoid synthesized by Deinococcus radiodurans, exhibits robust antioxidative activities in vitro and in vivo. The accumulation of excessive reactive oxygen species (ROS) and free radicals in the body would induce brain oxidative damage, thereby contributing to the process of aging. Whether the administration of DX could protect the brain against oxidative damage in aging is of great interest. In this study, we explored the potential beneficial effects of DX on D-galactose (D-gal)-induced aging mice in vivo, particularly its protective effects on the brain against oxidative damage, and its impact on the gut microbiota of aging mice. We demonstrated that treatment with a low dose (25 mg/kg/day) and a middle dose (50 mg/kg/day) of DX could effectively alleviate motor deficits, reduce the hippocampal pathological changes, suppress microglia and astrocyte activation, and attenuate oxidative stress in D-gal-induced aging mice. However, the treatment with a high dose of DX (100 mg/kg/day) seemed to exacerbate these changes, indicating that excessive DX may exacerbate oxidative damage in aging mice. Furthermore, the administration of appropriate DX could restore the gut microbiota in aging mice, while the high dose of DX further aggravated the disturbance of the gut microbiota in aging mice. Collectively, we conclude that taking DX appropriately may be beneficial in preventing oxidative damage to the brain and improving the gut microbiota in aging mice.
去甲氧基叶黄素(DX)是一种由耐辐射球菌合成的特殊羟基化四萜类化合物,在体外和体内均表现出强大的抗氧化活性。体内过量活性氧(ROS)和自由基的积累会导致脑氧化损伤,从而促进衰老进程。给予DX是否能保护大脑免受衰老过程中的氧化损伤备受关注。在本研究中,我们探讨了DX对D-半乳糖(D-gal)诱导的衰老小鼠体内的潜在有益作用,特别是其对大脑氧化损伤的保护作用以及对衰老小鼠肠道微生物群的影响。我们证明,低剂量(25mg/kg/天)和中剂量(50mg/kg/天)的DX治疗可有效缓解运动功能障碍,减少海马体病理变化,抑制小胶质细胞和星形胶质细胞活化,并减轻D-gal诱导的衰老小鼠的氧化应激。然而,高剂量DX(100mg/kg/天)治疗似乎会加剧这些变化,表明过量的DX可能会加剧衰老小鼠的氧化损伤。此外,给予适当剂量的DX可恢复衰老小鼠的肠道微生物群,而高剂量DX则进一步加剧了衰老小鼠肠道微生物群的紊乱。总的来说,我们得出结论,适当服用DX可能有助于预防衰老小鼠大脑的氧化损伤并改善其肠道微生物群。