Scholarlink

<p>This study evaluated the ameliorative effects of Heterophyllin J, a cyclic peptide derived from <i>Pseudostellaria heterophylla</i>, on lipopolysaccharide (LPS)-induced neuroinflammation in mice. Biochemical, and molecular analyses revealed that Heterophyllin J dose-dependently reduced hippocampal pro-inflammatory cytokines (IFN-γ, IL-1β, IL-6, TNF-α), suppressed oxidative stress (restoring glutathione and lowering malondialdehyde), and alleviated iron accumulation. Western blotting demonstrated Heterophyllin J downregulated NLRP3, Caspase1, and TLR4/NF-κB pathway proteins (COX-2, iNOS, Myd88) while enhancing antioxidant markers (Nrf2, HO-1, NQO1) via Keap1/Nrf2 activation. Heterophyllin J also modulated JAK/STAT signaling, restoring JAK1/2 phosphorylation and reducing STAT1/3 activation, thereby attenuating apoptosis (lower Bax, cleaved caspase-3; higher Bcl-2) and ferroptosis (upregulating GPX4, PCBP1, SLC40A1). These findings highlight Heterophyllin J’s multimodal mechanism: regulating TLR4-driven inflammation, rebalancing iron metabolism, and activating antioxidant pathways to counteract neuroinflammation. The results position Heterophyllin J as a promising therapeutic candidate for neurodegenerative diseases linked to neuroinflammatory and oxidative stress pathways.</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

Cyclopeptide heterophyllin from Pseudostellaria heterophylla alleviates neuroinflammation: a study integrating molecular dynamics, inflammatory pathway analysis, and in vivo validation

  • 期刊论文

  • 发表日期：

    2026年6月27日

查看全文
  • Bo Li,
  • Xueying Shi,
  • Erhua Chen,
  • Xianwen Chen

摘要

This study evaluated the ameliorative effects of Heterophyllin J, a cyclic peptide derived from Pseudostellaria heterophylla, on lipopolysaccharide (LPS)-induced neuroinflammation in mice. Biochemical, and molecular analyses revealed that Heterophyllin J dose-dependently reduced hippocampal pro-inflammatory cytokines (IFN-γ, IL-1β, IL-6, TNF-α), suppressed oxidative stress (restoring glutathione and lowering malondialdehyde), and alleviated iron accumulation. Western blotting demonstrated Heterophyllin J downregulated NLRP3, Caspase1, and TLR4/NF-κB pathway proteins (COX-2, iNOS, Myd88) while enhancing antioxidant markers (Nrf2, HO-1, NQO1) via Keap1/Nrf2 activation. Heterophyllin J also modulated JAK/STAT signaling, restoring JAK1/2 phosphorylation and reducing STAT1/3 activation, thereby attenuating apoptosis (lower Bax, cleaved caspase-3; higher Bcl-2) and ferroptosis (upregulating GPX4, PCBP1, SLC40A1). These findings highlight Heterophyllin J’s multimodal mechanism: regulating TLR4-driven inflammation, rebalancing iron metabolism, and activating antioxidant pathways to counteract neuroinflammation. The results position Heterophyllin J as a promising therapeutic candidate for neurodegenerative diseases linked to neuroinflammatory and oxidative stress pathways.