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Bufalin Inhibits Cytokine Storm by Regulating TLR4/TLR3 Signaling Pathway.

Xixi Liu1,2, Chencheng Li1,3, Jing Yang1

  • 1Affiliated Hospital of Nanjing University of Chinese Medicine, First Clinical Medical College of Nanjing University of Chinese Medicine, Nanjing, China.

Immunity, Inflammation and Disease
|February 5, 2026
PubMed
Summary
This summary is machine-generated.

Bufalin, a compound from toad venom, effectively reduces inflammation by inhibiting key signaling pathways. This research highlights bufalin

Keywords:
TOLL‐like receptorsbufalincytokine storminflammation

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Area of Science:

  • Pharmacology
  • Immunology
  • Traditional Chinese Medicine

Background:

  • Bufalin, a key component of Bufo gargarizans Cantor venom, possesses known anti-tumor and cardiotonic activities.
  • Research has largely overlooked bufalin's anti-inflammatory potential despite its historical use in traditional medicine.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of bufalin.
  • To elucidate the underlying molecular mechanisms of bufalin's anti-inflammatory action.

Main Methods:

  • Macrophages were stimulated with lipopolysaccharide (TLR4 ligand) and polyinosinic acid (TLR3 ligand) to induce inflammation.
  • Transcriptome sequencing and molecular experiments were employed to analyze the cellular response.
  • Molecular docking was used to predict potential drug targets.

Main Results:

  • Bufalin significantly decreased the production of pro-inflammatory factors including IL-6, TNF-α, and IL-1β.
  • The compound inhibited the phosphorylation of IKBα and IRF3, thereby down-regulating the Toll-like receptor (TLR) pathway.
  • Molecular docking identified MD-2 coupled with TLR4 as a potential target for bufalin.

Conclusions:

  • Bufalin demonstrates significant anti-inflammatory properties.
  • These findings validate the traditional use of toad venom for inflammatory conditions.
  • Bufalin represents a promising candidate for developing new anti-inflammatory therapeutics.