Scholarlink

<p>Attention deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder characterized by inattention, hyperactivity, and impulsivity, with limited effective treatments available. This study investigated the therapeutic potential of Dihydromyricetin (DMY) in a monosodium glutamate (MSG)-induced ADHD mouse model. Behavioral tests, including open field, Y-maze, and social interaction tests, were conducted to assess hyperactivity, attention, and social behavior. Molecular mechanisms were evaluated through Western blot analysis of oxidative stress markers (MDA, GPx, MPO) and key signaling proteins (SIRT1, Keap1, Nrf2, HO-1), as well as ELISA measurement of inflammatory cytokines (NF-κB, IL-6, TNF-α, IL-1β). Histological analysis assessed neuronal damage in the hippocampus and prefrontal cortex. Results showed that DMY treatment significantly improved ADHD-like behaviors, including reduced hyperactivity and enhanced attention and social interaction. It also restored oxidative balance by downregulating MPO, GPx and MDA levels. DMY modulated the SIRT1/Nrf2/Keap1/HO-1 pathway, attenuating inflammation and neuronal damage. These findings suggest that DMY alleviates ADHD symptoms by reducing oxidative stress and inflammation, highlighting its potential as a novel therapeutic agent for ADHD.</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

Dihydromyricetin alleviates attention deficit hyperactivity disorder by modulating the SIRT1/Nrf2/Keap1/HO-1 signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月9日

查看全文
  • Huanhuan Zang,
  • Dawei Yang,
  • Xiaoyun Yang,
  • Huaifu Dong,
  • Yucai Liu

摘要

Attention deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder characterized by inattention, hyperactivity, and impulsivity, with limited effective treatments available. This study investigated the therapeutic potential of Dihydromyricetin (DMY) in a monosodium glutamate (MSG)-induced ADHD mouse model. Behavioral tests, including open field, Y-maze, and social interaction tests, were conducted to assess hyperactivity, attention, and social behavior. Molecular mechanisms were evaluated through Western blot analysis of oxidative stress markers (MDA, GPx, MPO) and key signaling proteins (SIRT1, Keap1, Nrf2, HO-1), as well as ELISA measurement of inflammatory cytokines (NF-κB, IL-6, TNF-α, IL-1β). Histological analysis assessed neuronal damage in the hippocampus and prefrontal cortex. Results showed that DMY treatment significantly improved ADHD-like behaviors, including reduced hyperactivity and enhanced attention and social interaction. It also restored oxidative balance by downregulating MPO, GPx and MDA levels. DMY modulated the SIRT1/Nrf2/Keap1/HO-1 pathway, attenuating inflammation and neuronal damage. These findings suggest that DMY alleviates ADHD symptoms by reducing oxidative stress and inflammation, highlighting its potential as a novel therapeutic agent for ADHD.