# Protective Effects of Exogenous Donkey Oil on Skin Healing Under Incisional Wound Damage

**Authors:** Jie Yu, Lili Hu, Jie Cheng, Guangyuan Liu, Min Li, Wei Zhao, Jianping Huang, Hang Tie, Tao Wu, Hongyang Zhang, Bingguang Huang

PMC · DOI: 10.1111/jocd.70550 · Journal of Cosmetic Dermatology · 2025-11-18

## TL;DR

Donkey oil accelerates wound healing in mice by reducing inflammation and promoting tissue repair, suggesting it could be a valuable cosmetic ingredient.

## Contribution

This study demonstrates donkey oil's efficacy in wound healing through anti-inflammatory and tissue repair mechanisms, supported by transcriptomic and biochemical evidence.

## Key findings

- 25% and 50% donkey oil treatments accelerated wound closure by 35.22% and 34.33%, respectively.
- Donkey oil reduced inflammatory cell infiltration by 63.77% and 79.00% and inhibited MMP-9 while increasing VEGF.
- Transcriptome analysis revealed 13,603 differentially expressed genes linked to anti-inflammation and tissue repair pathways.

## Abstract

The identification of cosmetic ingredients that promote wound healing with minimal inflammation is urgently needed. Donkey oil (DO) is a promising candidate due to its nutritional richness and biosafety.

This study aimed to evaluate the efficacy of DO in promoting wound healing and to elucidate its underlying mechanisms of action.

A murine incisional wound model was established. Wounds were treated with 12.5%, 25%, or 50% DO. Healing was assessed through phenotypic observation, H&E staining, quantification of inflammatory cytokines (IL‐1α, IL‐6, PGE2, and CCL2) and VEGF, transcriptome sequencing, and qPCR validation.

Treatment with 25% and 50% DO significantly accelerated wound closure by 35.22% and 34.33%, respectively, and reduced inflammatory cell infiltration by 63.77% and 79.00%. Furthermore, DO preserved skin structural integrity, concurrently inhibited inflammatory cytokines increased VEGF levels, and reduced MMP‐9. To explore the potential mechanism, transcriptome analysis identified 13 603 shared differentially expressed genes (DEGs). Subsequent GO and KEGG enrichment analyses indicated these DEGs were involved in key processes like actin cytoskeleton organization and pathways related to anti‐infection and cell repair. Finally, qPCR confirmed the reversal of IL‐6 and CCL2 expression and the upregulation of TGF‐α.

DO significantly promotes wound healing by modulating anti‐inflammatory responses and enhancing tissue repair mechanisms, demonstrating its great potential as an effective cosmetic ingredient.

## Linked entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552], IL6 (interleukin 6) [NCBI Gene 3569], ptges2.L (prostaglandin E synthase 2 L homeolog) [NCBI Gene 100037123], CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347], VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422], MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318], TGFA (transforming growth factor alpha) [NCBI Gene 7039]
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Tgfa (transforming growth factor alpha) [NCBI Gene 21802] {aka wa-1, wa1}, Il1a (interleukin 1 alpha) [NCBI Gene 16175] {aka Il-1a}, Vegfa (vascular endothelial growth factor A) [NCBI Gene 22339] {aka L-VEGF, Vegf, Vpf}, Mmp9 (matrix metallopeptidase 9) [NCBI Gene 17395] {aka B/MMP9, Clg4b, Gel B, MMP-9, pro-MMP-9}, Ccl2 (C-C motif chemokine ligand 2) [NCBI Gene 20296] {aka HC11, JE, MCAF, MCP-1, MCP1, SMC-CF}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}
- **Diseases:** inflammation (MESH:D007249), infection (MESH:D007239), Wound Damage (MESH:D014947)
- **Chemicals:** H&amp;E (MESH:D006371), DO (-)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12626390/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12626390/full.md

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Source: https://tomesphere.com/paper/PMC12626390