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Related Experiment Video

Updated: Sep 12, 2025

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

Emodin Alleviates Sepsis-Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL-10.

Xiaolong Xu¹, Yumeng Yan^1,2, Meiling Zheng¹

¹Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Institute of Chinese Medicine, Beijing Key Laboratory of Basic Research with Traditional Chinese Medicine on Infectious Diseases, Beijing, 100010, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|August 8, 2025

Summary

Emodin, a natural compound, effectively treats sepsis by inhibiting neutrophil extracellular traps (NETs) formation. It targets BCL-10, modulating the BCL-10/MALT1 complex to reduce inflammation and protect organs.

Keywords:

BCL‐10/MALT1 Emodin NETosis NF‐κB sepsis

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Last Updated: Sep 12, 2025

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

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Published on: December 9, 2022

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

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Published on: June 15, 2019

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

Published on: January 27, 2019

Area of Science:

Biochemistry
Immunology
Pharmacology

Background:

Sepsis involves excessive inflammation and abnormal coagulation.
Neutrophil extracellular traps (NETs) link inflammation and coagulation in sepsis.
Emodin, from Dahuang, is a potential therapeutic agent.

Purpose of the Study:

To investigate Emodin's therapeutic effects on sepsis.
To identify Emodin's molecular target in sepsis.
To elucidate the mechanism of Emodin's action.

Main Methods:

In vivo and in vitro sepsis models.
Protein microarrays, SPR, pull-down assays, molecular docking.
Conditional BCL-10 knockout in neutrophils, single-cell sequencing.

Main Results:

Emodin ameliorates sepsis-induced cytokine storm and coagulation abnormalities.
Emodin directly targets BCL-10, inhibiting NETs formation.
BCL-10 promotes excessive NET formation in sepsis.
Emodin modulates the BCL-10/MALT1 complex, suppressing NF-κB activation.

Conclusions:

Emodin targets BCL-10 to regulate the BCL-10/MALT1 complex and NF-κB signaling.
Emodin confers significant multiorgan protection in sepsis.
Findings support Emodin's translational research potential for sepsis treatment.