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<p>Toll-like receptors (TLRs) are key mediators of innate immune responses, and their dysregulation contributes to inflammatory diseases. Dehydroandrographolide (DAG), a diterpene lactone from <i>Andrographis paniculata</i>, is known for its anti-inflammatory activity, but its effects on individual branches of TLR signaling remain unclear. RAW264.7 and 293T cells were used to evaluate the effects of DAG on MyD88- and TRIF-dependent signaling pathways. Luciferase reporter assays, Western blotting, RT-PCR, and nitrite assays were employed to assess NF-κB and IRF3 activation and inflammatory mediator expression. Statistical analysis was performed using one-way ANOVA. DAG significantly inhibited activation of NF-κB and IRF3 induced by TLR agonists (LPS, MALP-2, and Poly[I:C]) and by overexpression of MyD88- and TRIF-associated downstream molecules. Correspondingly, DAG suppressed iNOS, IFNβ, and IP-10 expression, indicating dual inhibition of both TLR signaling branches. DAG exerts dual inhibitory effects on MyD88- and TRIF-dependent TLR signaling, attenuating inflammatory mediator expression. DAG may represent a promising molecular scaffold or mechanistic candidate for modulating TLR-mediated inflammatory signaling.</p>

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Dehydroandrographolide attenuates Toll-like receptor signaling by dual inhibition of MyD88- and TRIF-dependent pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月16日

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  • Ye Eun Lee,
  • Hanbin Ko,
  • Dongwoo Lee,
  • Ha Eun Park,
  • Seo-Yeong Kim,
  • Gyuri Park,
  • Seonah Kim,
  • Younghyun Lee,
  • Hyung-Sun Youn,
  • Gyo Jeong Gu

摘要

Toll-like receptors (TLRs) are key mediators of innate immune responses, and their dysregulation contributes to inflammatory diseases. Dehydroandrographolide (DAG), a diterpene lactone from Andrographis paniculata, is known for its anti-inflammatory activity, but its effects on individual branches of TLR signaling remain unclear. RAW264.7 and 293T cells were used to evaluate the effects of DAG on MyD88- and TRIF-dependent signaling pathways. Luciferase reporter assays, Western blotting, RT-PCR, and nitrite assays were employed to assess NF-κB and IRF3 activation and inflammatory mediator expression. Statistical analysis was performed using one-way ANOVA. DAG significantly inhibited activation of NF-κB and IRF3 induced by TLR agonists (LPS, MALP-2, and Poly[I:C]) and by overexpression of MyD88- and TRIF-associated downstream molecules. Correspondingly, DAG suppressed iNOS, IFNβ, and IP-10 expression, indicating dual inhibition of both TLR signaling branches. DAG exerts dual inhibitory effects on MyD88- and TRIF-dependent TLR signaling, attenuating inflammatory mediator expression. DAG may represent a promising molecular scaffold or mechanistic candidate for modulating TLR-mediated inflammatory signaling.