Scholarlink

<p>Alzheimer’s disease (AD) is the leading type of dementia, characterized by the gradual worsening of memory, disruption in synaptic communication, and progressive death of nerve cells. Pathological hallmarks of AD include the accumulation of amyloid‑β plaques, abnormal hyperphosphorylation of tau protein, increased oxidative stress, and persistent neuroinflammation. These factors collectively contribute to the initiation and advancement of the disease. Among the cellular signaling pathways involved, the nuclear factor erythroid 2‑related factor&#xa0;2 (Nrf-2) and nuclear factor kappa-light-chain-enhancer of activated B&#xa0;cells (NF-κB) pathways serve as major regulators, with Nrf‑2 chiefly controlling oxidative stress and NF-κB primarily managing inflammatory responses. These pathways work in dynamic balance to modulate cellular defense mechanisms. Disruption in this balance can contribute to disease pathology by increasing oxidative damage and neuroinflammation. Sinigrin is a&#xa0;naturally occurring glucosinolate predominantly found in cruciferous vegetables like broccoli and brussel sprouts. Preclinical studies indicate that Sinigrin regulates the Nrf-2/NF-κB signaling axis in a&#xa0;dual manner. Activation of Nrf‑2 by Sinigrin leads to an increased production of protective antioxidant enzymes such as heme oxygenase‑1 (HO-1) and NAD(P)H quinone oxidoreductase&#xa0;1 (NQO1), which helps to diminish oxidative stress. Sinigrin simultaneously blocks the activation of NF-κB, which results in the decreased production of pro-inflammatory cytokines like TNF‑α, IL-1β, and IL‑6. This review emphasizes the therapeutic importance of Sinigrin in AD, with a&#xa0;special focus on its ability to modulate the interplay between the Nrf‑2 and NF-κB signaling pathways. This dual action helps protect brain cells from damage and supports overall neural health.</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

Sinigrin as a dual modulator of oxidative stress and neuroinflammation: Targeting Nrf-2-NF-κB crosstalk in Alzheimer’s disease

  • 期刊论文

  • 发表日期：

    2025年4月1日

查看全文
  • Sanchi Jain,
  • Romanpreet Kaur,
  • Shamsher Singh

摘要

Alzheimer’s disease (AD) is the leading type of dementia, characterized by the gradual worsening of memory, disruption in synaptic communication, and progressive death of nerve cells. Pathological hallmarks of AD include the accumulation of amyloid‑β plaques, abnormal hyperphosphorylation of tau protein, increased oxidative stress, and persistent neuroinflammation. These factors collectively contribute to the initiation and advancement of the disease. Among the cellular signaling pathways involved, the nuclear factor erythroid 2‑related factor 2 (Nrf-2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways serve as major regulators, with Nrf‑2 chiefly controlling oxidative stress and NF-κB primarily managing inflammatory responses. These pathways work in dynamic balance to modulate cellular defense mechanisms. Disruption in this balance can contribute to disease pathology by increasing oxidative damage and neuroinflammation. Sinigrin is a naturally occurring glucosinolate predominantly found in cruciferous vegetables like broccoli and brussel sprouts. Preclinical studies indicate that Sinigrin regulates the Nrf-2/NF-κB signaling axis in a dual manner. Activation of Nrf‑2 by Sinigrin leads to an increased production of protective antioxidant enzymes such as heme oxygenase‑1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which helps to diminish oxidative stress. Sinigrin simultaneously blocks the activation of NF-κB, which results in the decreased production of pro-inflammatory cytokines like TNF‑α, IL-1β, and IL‑6. This review emphasizes the therapeutic importance of Sinigrin in AD, with a special focus on its ability to modulate the interplay between the Nrf‑2 and NF-κB signaling pathways. This dual action helps protect brain cells from damage and supports overall neural health.