Scholarlink

<p>Deinoxanthin (DX), a special hydroxylated tetraterpenoid synthesized by <i>Deinococcus radiodurans</i>, 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&#xa0;mg/kg/day) and a middle dose (50&#xa0;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&#xa0;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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Protective Effects of Deinoxanthin on Brain Oxidative Damage and Gut Microbiota in the D-Galactose-Induced Aging Mice

  • 期刊论文

  • 发表日期：

    2025年7月19日

查看全文
  • Huijuan Su,
  • Yutao Li,
  • Jiayi Wan,
  • Jieyu Lin,
  • Jiayao Wang,
  • Rui Fan,
  • Dingming Liu,
  • Jing Wei,
  • Hongbo Xin,
  • Yuejin Hua,
  • Shengjie Li

摘要

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.