# Exploration of the Therapeutic Protocols and Underlying Molecular Mechanisms of Autologous Platelet‐Rich Plasma in the Treatment of Deep Second‐Degree Burns

**Authors:** Jian‐Guo Shi, Wei Liu, Hong‐Qiang Liu, Dan Rao, Jun‐Wei Huang, Yu‐Fei Zhao

PMC · DOI: 10.1111/jocd.70751 · Journal of Cosmetic Dermatology · 2026-02-25

## TL;DR

This study explores how different platelet-rich plasma (PRP) treatment protocols affect healing in deep second-degree burns and finds that early application and leukocyte-poor PRP improve outcomes.

## Contribution

The study identifies optimal PRP treatment protocols and their molecular mechanisms for deep second-degree burns.

## Key findings

- PRP treatment improves wound healing time, wound coverage, and scar outcomes compared to controls.
- Early PRP intervention and leukocyte-poor PRP enhance healing by promoting M2 macrophage polarization.
- High-frequency PRP does not improve outcomes and may hinder healing due to excessive TGF-β.

## Abstract

Platelet‐rich plasma (PRP) has been widely applied in burn wound management due to its high concentration of bioactive growth factors. However, inconsistent clinical outcomes and the lack of standardized protocols regarding timing, frequency, and leukocyte content limit its broader clinical adoption.

This study aimed to evaluate the therapeutic efficacy of PRP under different application protocols in patients with deep second‐degree burns and to explore the underlying molecular mechanisms, with the goal of informing standardized, evidence‐based PRP treatment strategies.

Thirty‐three patients with deep second‐degree burns were enrolled and randomly assigned to five groups: a standard PRP group, a saline control group, an early intervention PRP group, a high‐frequency PRP group, and a leukocyte‐poor PRP group. Clinical outcomes included wound healing time, wound coverage rates at 2 and 3 weeks, bacterial culture positivity, and Vancouver Scar Scale scores at 3 months. Wound tissue and exudate samples were collected at predefined time points for immunohistochemical analysis of macrophage phenotypes (M1/M2) and quantification of growth factors (VEGF, PDGF, TGF‐β).

Compared with the control group, PRP treatment was associated with a shorter wound healing time, increased early wound coverage, reduced bacterial culture positivity, and improved scar outcomes. Early PRP intervention and the use of leukocyte‐poor PRP appeared to further enhance healing efficiency, which may be related to accelerated polarization of macrophages from the pro‐inflammatory M1 phenotype toward the anti‐inflammatory M2 phenotype. In contrast, high‐frequency PRP administration resulted in higher local growth factor levels but did not translate into additional clinical benefit; this lack of efficacy may be attributable to excessive expression of transforming growth factor‐β (TGF‐β), which could potentially counteract optimal tissue repair.

PRP is an effective adjunctive therapy for small‐area deep second‐degree burns. Early application and leukocyte‐poor PRP appear optimal, whereas indiscriminately increasing treatment frequency is not recommended. Controlled modulation of PRP‐derived growth factors may be key to maximizing therapeutic benefit.

## Linked entities

- **Proteins:** VEGFA (vascular endothelial growth factor A), pdgfa.S (platelet derived growth factor subunit A S homeolog), TGFB1 (transforming growth factor beta 1), CHRM1 (cholinergic receptor muscarinic 1), M2 (matrix protein 2)

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, MMP3 (matrix metallopeptidase 3) [NCBI Gene 4314] {aka CHDS6, MMP-3, SL-1, STMY, STMY1, STR1}, EGF (epidermal growth factor) [NCBI Gene 1950] {aka HOMG4, URG}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, ISYNA1 (inositol-3-phosphate synthase 1) [NCBI Gene 51477] {aka INO1, INOS, IPS, IPS 1, IPS-1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, MRC1 (mannose receptor C-type 1) [NCBI Gene 4360] {aka CD206, CLEC13D, CLEC13DL, MMR, MRC1L1, bA541I19.1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** diabetes mellitus (MESH:D003920), malignancy (MESH:D009369), Neurological or psychiatric disorders (MESH:D001523), pain (MESH:D010146), fibrosis (MESH:D005355), systemic infection (MESH:D012141), Wounds (MESH:D014947), Chronic inflammation (MESH:D007249), Burn injuries (MESH:D002056), osteoarthritis (MESH:D010003), scar (MESH:D002921), autoimmune disorders (MESH:D001327), scar hypertrophy (MESH:D006984), Thrombocytopenia (MESH:D013921), infected (MESH:D007239), deaths (MESH:D003643), Hypoproteinemia (MESH:D007019), hypertrophic scar (MESH:D017439), cognitive impairment (MESH:D003072), MRSA (MESH:D013203), necrotic (MESH:D009336), Osteomyelitis (MESH:D010019), cardiac, hepatic, or renal dysfunction (MESH:D006331), deep partial-thickness (deep second-degree) burns (MESH:D057887), IDD (MESH:D055959), bacterial infection (MESH:D001424)
- **Chemicals:** silver (MESH:D012834), sodium citrate (MESH:D000077559), Lp-PRP (-), povidone-iodine (MESH:D011206), LP (MESH:D008070)
- **Species:** Klebsiella pneumoniae (species) [taxon 573], Mus musculus (house mouse, species) [taxon 10090], Escherichia coli (E. coli, species) [taxon 562], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116], Staphylococcus aureus (species) [taxon 1280], Streptococcus (genus) [taxon 1301]
- **Mutations:** A > F, A > E, G > A

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12933696/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12933696/full.md

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Source: https://tomesphere.com/paper/PMC12933696