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Abstract

Background/purpose:

Periodontal inflammation contributes to endothelial dysfunction, but effective biologically active strategies for vascular protection remain limited. This study investigated whether deer antler tip cell culture supernatant could rescue Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) induced endothelial injury and restore endothelial homeostasis.

Materials and methods:

Velvet antler tissues from the tip, shaft, and burr regions were examined histologically and used for primary cell isolation. Human umbilical vein endothelial cells were exposed to Pg-LPS or indirectly co-cultured with LPS-stimulated THP-1-derived macrophages. Deer antler tip cell culture supernatant was subsequently applied to these endothelial inflammatory models, and its protective effects were assessed by quantitative functional assays, Western blotting, and qPCR. Public venous thromboembolism transcriptomic datasets were analyzed to evaluate the translational relevance of the endothelial injury and repair signatures.

Results:

The antler tip showed a vascular-rich regenerative niche with stem/progenitor-associated features. In HUVECs, Pg-LPS induced inflammatory activation, oxidative stress, and endothelial dysfunction, whereas deer antler tip cell culture supernatant attenuated these changes. It also suppressed macrophage-mediated endothelial injury and reduced Pg-LPS induced inflammatory activation in THP-1-derived macrophages. In an optimized endothelial injury model, deer antler tip cell culture supernatant dose-dependently restored endothelial homeostasis- and mechanosensitive-associated gene expression. Public datasets further supported the translational relevance of these endothelial stress signatures.

Conclusion:

Deer antler tip cell culture supernatant protects against Pg-LPS associated endothelial inflammatory injury and may serve as a promising biologically active strategy for vascular protection.

Publication Date

2026

Received Date

May 18 2026

Accepted Date

June 3 2026

Final Revision Date

June 3 2026

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