Saved in:
| Main Authors: | , , , , , , , , , |
|---|---|
| Format: | Artículo científico |
| Language: | en |
| Published: |
Food & function
2025
|
| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/40197680/ |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Table of Contents:
- Ketogenic diet attenuates neuroinflammation and restores hippocampal neurogenesis to improve CUMS induced depression-like behavior in mice. Liang, Jinyuan Zhang, Jingxi Sun, Jingyu Liang, Qingsheng Zhan, Yingtong Yang, Zhiyou Zhang, Yongping Jin, Leigang Hu, Chuanyin Zhao, Yun-Tao Animals Diet, Ketogenic Neurogenesis Mice Hippocampus Depression Male Neuroinflammatory Diseases Behavior, Animal Doublecortin Protein Stress, Psychological Toll-Like Receptor 4 Mice, Inbred C57BL Disease Models, Animal Brain-Derived Neurotrophic Factor The ketogenic diet (KD) has been proposed as a potential treatment for depression. However, the underlying mechanisms remain poorly understood. This study aimed to evaluate further the effects of KD on chronic unpredictable mild stress (CUMS)-induced depression in mice and investigate the underlying mechanisms. The results demonstrated that KD intervention significantly alleviated CUMS-induced depression-like behaviors, as evidenced by a decrease in immobility time in the forced swimming test and tail suspension test, an increase in distance traveled in the open field test, and a greater preference for sucrose in the sucrose preference test. KD alleviated neuroinflammation by reducing the levels of glial cell activation markers Iba-1 and GFAP, inhibiting the expression of inflammatory factors IL-1β, TNF-α, and COX-2, and suppressing the overactivation of the TLR4/MyD88/NF-κB signaling pathway. Furthermore, KD increased the number of DCX-, BrdU-, and PSD95-positive cells in the hippocampus and enhanced the BDNF/TrkB/CREB and Wnt/β-catenin signaling pathways, thereby promoting hippocampal neurogenesis. These findings suggested that KD alleviated CUMS-induced depression-like behaviors in mice by reducing neuroinflammation, enhancing neurotrophic signaling, and promoting hippocampal neurogenesis, thereby providing a mechanistic basis for its potential as a novel dietary antidepressant therapy.