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<p>Excessive inflammation and oxidative stress can accelerate inflammatory disease. Plant exosome-like nanoparticles demonstrate therapeutic capacity for anti-inflammatory and antioxidant effects. Here, the effects of red cabbage exosome-like nanoparticles (RELNs) on inflammation and oxidative stress triggered by LPS in macrophages were investigated. RELNs inhibited the expression of the TLR4/NF-κB pathway and blocked the entry of NF-κB p65 from the cytoplasm into the nucleus. Additionally, RELNs reduced the ROS level, alleviated oxidative damage in mitochondria, and increased antioxidant enzyme activity in macrophages. Importantly, RELNs promoted the expression of the Nrf2/Keap1 pathway-mediated antioxidant genes and increased the entry of Nrf2 from the cytoplasm into the nucleus. The research further demonstrated that RELNs might be dependent on Nrf2 expression to decrease the inflammatory response. In brief, RELNs could reduce LPS-induced macrophage inflammation and oxidative stress in vitro, suggesting the therapeutic potential of RELNs in clinical inflammatory diseases.</p> Graphic abstract <p></p>

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Red cabbage exosome-like nanoparticles inhibited LPS-induced inflammation and oxidative stress in RAW264.7 cells

  • 期刊论文

  • 发表日期：

    2025年6月13日

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  • Jie Cao,
  • Jing Zhang,
  • Ling Yan,
  • Changhong Liu,
  • Yaqian Wang,
  • Yaqi Cao,
  • Lei Zheng

摘要

Excessive inflammation and oxidative stress can accelerate inflammatory disease. Plant exosome-like nanoparticles demonstrate therapeutic capacity for anti-inflammatory and antioxidant effects. Here, the effects of red cabbage exosome-like nanoparticles (RELNs) on inflammation and oxidative stress triggered by LPS in macrophages were investigated. RELNs inhibited the expression of the TLR4/NF-κB pathway and blocked the entry of NF-κB p65 from the cytoplasm into the nucleus. Additionally, RELNs reduced the ROS level, alleviated oxidative damage in mitochondria, and increased antioxidant enzyme activity in macrophages. Importantly, RELNs promoted the expression of the Nrf2/Keap1 pathway-mediated antioxidant genes and increased the entry of Nrf2 from the cytoplasm into the nucleus. The research further demonstrated that RELNs might be dependent on Nrf2 expression to decrease the inflammatory response. In brief, RELNs could reduce LPS-induced macrophage inflammation and oxidative stress in vitro, suggesting the therapeutic potential of RELNs in clinical inflammatory diseases.

Graphic abstract