Tectorigenin promotes skin flap survival by downregulating the TLR4-NF-κB signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Flap necrosis remains a major challenge in flap transplantation. Shegan, a traditional Chinese medicine, is known for its heat-clearing, detoxifying properties,blood-activating and removing blood stasis. Its principal bioactive compound, tectorigenin, has shown protective effects against skin damage, yet its influence on flap survival has not been fully elucidated.

MATERIALS AND

METHODS

A modified McFarlane random skin flap model was established in rats, which were divided into high-dose, low-dose, and control groups. After 7 days of treatment, flap survival rate was evaluated. Angiogenesis and perfusion were assessed using gelatin-lead oxide angiography and laser Doppler flowmetry. Zone II flap tissues were analyzed histologically via hematoxylin and eosin staining. Oxidative stress was evaluated through malondialdehyde (MDA) content, superoxide dismutase (SOD) glutathione peroxidase (GSH-Px) activity and reactive oxygen species (ROS). Immunohistochemistry and Immunofluorescence were performed to detect the expression of vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and Platelet endothelial cell adhesion molecule-1 (CD31). Western blotting was used to assess Toll-like receptor 4 (TLR4), Nuclear transcription factor (NF-κB), B-cell lymphoma-2 (Bcl-2), and BCL2-Associated X (BAX) expression levels.

RESULTS

Tectorigenin significantly improved skin flap survival, enhanced angiogenesis, and increased blood perfusion. It elevated VEGF and CD31 expression and SOD and GSH-Px activity while reducing MDA levels, inflammatory cytokines, and neutrophil infiltration. Furthermore, it suppressed TLR4 and NF-κB signaling and modulated Bcl-2 and BAX expression to inhibit apoptosis.

CONCLUSION

Tectorigenin enhances skin flap survival by promoting angiogenesis and suppressing inflammation, oxidative stress, and apoptosis, potentially via inhibition of the TLR4-NF-κB pathway.