ArticleApplied biochemistry and biotechnology2026
DianDao San Promotes CSU Wound Healing by Inhibiting TNF/NF-κB Pathway.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic Skin Ulcer (CSU) is a refractory wound arrested in persistent inflammation, preventing normal transition to the proliferative phase. DianDao San (DDS), a topical Chinese herbal formula composed of rhubarb and sulfur (1:1), is used for various skin diseases, but its molecular mechanism remains unclear. This study aims to elucidate the mechanism by which DDS promotes CSU healing.
methodsNetwork pharmacology analysis was used to predict the core targets and pathways of DDS in CSU. A rat CSU model was established to record wound healing rates. HE and Masson staining observed tissue morphology, while ELISA and Western Blot detected key protein expressions in the wound. An inflammatory model was built using TNF-α-induced human immortalized keratinocytes. EdU and MTT assays evaluated cell viability and proliferation, and scratch and Transwell assays assessed cell migration.
resultsNetwork pharmacology suggested TNF and NF-κB signaling pathways as core potential targets of DDS. Animal experiments showed DDS accelerated chronic ulcer healing, promoted re-epithelialization and granulation tissue formation, and regulated relevant protein levels. In vitro, DDS inhibited NF-κB activation, reduced MMP9 expression, upregulated Ki67, and promoted keratinocyte proliferation and migration, effects reversible by NF-κB agonist LPS.
conclusionThis study confirms DDS accelerates CSU healing by inhibiting the TNF-α/NF-κB signaling axis, reducing extracellular matrix degradation, and promoting keratinocyte proliferation and migration, providing clear molecular pharmacological evidence for its clinical efficacy.
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