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Updated: Dec 21, 2025

Rat Burn Model to Study Full-Thickness Cutaneous Thermal Burn and Infection
Published on: August 23, 2022
Camellia cake extracts reduce burn injury through suppressing inflammatory responses and enhancing collagen synthesis
Yuxia Liu1, Xiaomei Xiao2,3, Luling Ji2
1Center for Immunology, Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, Ganzhou, Jiangxi, China.
Background:
Burn injury accidents happen in our daily life, and the burn mortality is especially high in the low-to-middle-income countries. Camellia cake extracts (CCEs) are compound extracts from Camellia cake, and the major ingredients in CCEs may have antimicrobial, anti-oxidative, and anti-inflammatory effects. However, the effects of CCEs on burn inflammation and injury remain unknown.
Objective:
This study is to investigate the effects of CCEs in burn injury and explore its mechanism.
Design:
First, CCEs were identified to mainly contain camelliaside A and B using Ultra High Performance Liquid Chromatography-Time of Flight Mass Spectrometer (UHPLC-TOF-MS) method. Second, the CCEs' effect on burn was tested. Burn was induced by boiling water in mice, and then CCEs (30, 50, and 100 mg/mL) were applied on the damaged skin at 3, 7, and 14 days after burn induction.
Results:
The results showed that CCEs protected the skin from burn-induced inflammation and enhanced the wound healing in a dose-dependent manner. CCEs decreased the expression levels of various cytokines including IL-6, TNF-α, IL-1β, MCP-1, TGF-β, and IL-10, as well as inflammatory related factors iNOS. Moreover, CCEs increased the levels of collagens, including the mRNA of COLα-1 and COL-3, and inhibited the mRNA of MMP-1 and TIMP-1, and increased the collagen staining. CCEs also reversed the impairment of activity levels of anti-oxidative enzymes. Furthermore, CCEs suppressed the gene expression of pro-inflammatory cytokines in LPS-stimulated human skin keratinocyte, possibly through inhibiting NF-κB signaling pathway. In addition, toxicological safety experiments on CCEs showed that the oral median lethal dose (LD50) was 2,000 mg/kg, the percutaneous LD50 was greater than 2,000 mg/kg, and CCEs did not cause gene mutation.
Conclusion:
CCEs exert a potent anti-inflammatory effect against burn damage in mice. And toxicological safety experiments suggest that CCEs are safe for usage.
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