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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...

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Related Experiment Video

Updated: Jul 3, 2026

Demonstration of the Rat Ischemic Skin Wound Model
08:35

Demonstration of the Rat Ischemic Skin Wound Model

Published on: April 1, 2015

DianDao San Promotes CSU Wound Healing by Inhibiting TNF/NF-κB Pathway.

Linbo Sun1, Chen Cai2, Ming He2

  • 1Department of Dermatology, The First Clinical Medical College of Guizhou, University of Traditional Chinese Medicine, No. 71, Baoshan North Road, Yunyan District, Guizhou Province, 550000, Guiyang City, China. sunlinbo520@163.com.

Applied Biochemistry and Biotechnology
|July 2, 2026
PubMed
Summary
This summary is machine-generated.

DianDao San (DDS) accelerates chronic skin ulcer healing by inhibiting inflammation and promoting cell growth. This traditional Chinese herbal formula targets the TNF-α/NF-κB pathway for effective wound repair.

Keywords:
Chronic Skin Ulcers (CSU)DianDao San (DDS)InflammationNetwork pharmacologyTNF-α/NF-κB pathway

Related Experiment Videos

Last Updated: Jul 3, 2026

Demonstration of the Rat Ischemic Skin Wound Model
08:35

Demonstration of the Rat Ischemic Skin Wound Model

Published on: April 1, 2015

Area of Science:

  • Dermatology
  • Pharmacology
  • Molecular Biology

Background:

  • Chronic skin ulcers (CSUs) are difficult-to-heal wounds stuck in inflammation.
  • The molecular mechanisms of topical Chinese herbal formulas like DianDao San (DDS) for CSUs are unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism of DianDao San (DDS) in promoting chronic skin ulcer (CSU) healing.

Main Methods:

  • Network pharmacology identified core targets and pathways.
  • Rat CSU models and TNF-α-induced keratinocyte models were used.
  • Histology, ELISA, Western Blot, EdU, MTT, scratch, and Transwell assays assessed healing and cellular responses.

Main Results:

  • DDS accelerated CSU healing, promoting re-epithelialization and granulation tissue formation in vivo.
  • DDS inhibited TNF-α/NF-κB signaling, reduced MMP9, and upregulated Ki67 in vitro.
  • DDS enhanced keratinocyte proliferation and migration, with effects modulated by NF-κB activation.

Conclusions:

  • DDS accelerates CSU healing by inhibiting the TNF-α/NF-κB signaling axis.
  • DDS reduces extracellular matrix degradation and promotes keratinocyte proliferation and migration.
  • This study provides molecular evidence for the clinical efficacy of DDS in treating chronic skin ulcers.