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<p>Neuroinflammation is a critical pathological process underlying many neurological disorders, driven by activated glia and pro-inflammatory cytokine release. This study developed a novel functionalized gold nanocomposite drug (EF-PEG-GNPs) to be associated with the modulation of this process. The synthesized EF-PEG-GNPs (8.2 ± 1.3&#xa0;nm) exhibited excellent colloidal stability and minimal cytotoxicity, maintaining cell viability &gt;90% at concentrations up to 50&#xa0;μg/mL in human SVGp12 glial cells. Efficient cellular uptake was confirmed by TEM and ICP-MS, showing time-dependent internalization reaching saturation at 24&#xa0;h. In a lipopolysaccharide (LPS)-induced inflammatory model, EF-PEG-GNPs significantly mitigated reactive astrogliosis morphological changes and suppressed the mRNA expression of key cytokines, reducing IL-1β and TNF-α levels by approximately 43% and 39%, respectively, compared to the LPS group. Furthermore, they reduced LPS-induced apoptosis. Mechanistic investigations revealed that these effects were mediated through the inhibition of the TAB1-NF-κB signaling pathway, evidenced by downregulation of TAB1 suppressed phosphorylation of IKKα/β and NF-κBp65, and altered IκBα phosphorylation dynamics. These results demonstrate that EF-PEG-GNPs are a highly promising anti-inflammatory nanotherapeutic agent capable of modulating critical neuroinflammatory pathways, offering a significant potential strategy for treating neuroinflammatory conditions.</p>

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Gold nanoparticles modulate the TAB1-NF-κB signaling pathway to ameliorate lipopolysaccharide-induced inflammatory response in astrocytes

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Zeqiang Sun,
  • Xiaomin Wei,
  • Fuzhen Yang,
  • Wenli Zheng

摘要

Neuroinflammation is a critical pathological process underlying many neurological disorders, driven by activated glia and pro-inflammatory cytokine release. This study developed a novel functionalized gold nanocomposite drug (EF-PEG-GNPs) to be associated with the modulation of this process. The synthesized EF-PEG-GNPs (8.2 ± 1.3 nm) exhibited excellent colloidal stability and minimal cytotoxicity, maintaining cell viability >90% at concentrations up to 50 μg/mL in human SVGp12 glial cells. Efficient cellular uptake was confirmed by TEM and ICP-MS, showing time-dependent internalization reaching saturation at 24 h. In a lipopolysaccharide (LPS)-induced inflammatory model, EF-PEG-GNPs significantly mitigated reactive astrogliosis morphological changes and suppressed the mRNA expression of key cytokines, reducing IL-1β and TNF-α levels by approximately 43% and 39%, respectively, compared to the LPS group. Furthermore, they reduced LPS-induced apoptosis. Mechanistic investigations revealed that these effects were mediated through the inhibition of the TAB1-NF-κB signaling pathway, evidenced by downregulation of TAB1 suppressed phosphorylation of IKKα/β and NF-κBp65, and altered IκBα phosphorylation dynamics. These results demonstrate that EF-PEG-GNPs are a highly promising anti-inflammatory nanotherapeutic agent capable of modulating critical neuroinflammatory pathways, offering a significant potential strategy for treating neuroinflammatory conditions.