Inhibitory effects of different concentrations of auranofin on M1 macrophage function and its therapeutic potential in diabetic wound healing
10.12307/2026.555
- VernacularTitle:不同浓度金诺芬抑制M1型巨噬细胞功能及修复糖尿病小鼠伤口的价值
- Author:
Hongfei PAN
1
;
Zhenbing ZHUANG
;
Baiyun XU
;
Zhangyang YANG
;
Kairui LIN
;
Bingqing ZHAN
;
Jinghan LAN
;
Heng GAO
;
Nanbo ZHANG
;
Jiayu LIN
Author Information
1. 福建医科大学,福建省 福州市 350000
- Publication Type:Journal Article
- Keywords:
auranofin;
M1 Macrophages;
diabetes mellitus;
skin defects;
inflammatory factors;
wound healing;
engineered tissue construction
- From:
Chinese Journal of Tissue Engineering Research
2026;30(6):1390-1397
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:During diabetic wound healing,the sustained activation of M1 macrophages exacerbates the inflammatory response and hinders wound repair.Auranofin,an anti-inflammatory drug,has not been clearly studied for its effects on M1 macrophages and its potential role in diabetic wound healing.OBJECTIVE:To investigate the effects of different concentrations of auranofin on the biological function of M1 macrophages and evaluate its potential application in diabetic wound healing.METHODS:RAW264.7 and THP-1 cells were used as research models.M1 polarization was induced using different concentrations of interferon-γ and lipopolysaccharide.M1 macrophages were treated with 1 and 2 μmol/L auranofin.Cell counting kit-8 assay was used to evaluate the effect of auranofin on cell viability.Quantitative real-time PCR was performed to detect mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.ELISA was employed to measure the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-α in the supernatant.Western blot analysis was used to assess the expression of nuclear factor-κB(p65),phosphorylated mitogen-activated protein kinases(MAPK),and total MAPK proteins.Additionally,6-8-week-old male C57BL/6J and db/db diabetic mice were used for wound healing experiments,with the mice divided into C57 control,db/db control and auranofin treatment groups,each containing six animals.Dorsal skin defect modeling and treatment with intraperitoneal injection of auranofin were performed to observe wound healing in mice.RESULTS AND CONCLUSION:(1)Cell experiments showed that co-treatment with interferon-y(10 ng/mL)and lipopolysaccharide(100 ng/mL)significantly induced M1 polarization in RAW264.7 and THP-1 cells,resulting in increased mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.Treatment with auranofin(1 and 2 μmol/L)reduced the mRNA expression of these inflammatory factors in the cells and inhibited the secretion of inflammatory factors in the cell supernatant.(2)Auranofin treatment significantly suppressed the activation of nuclear factor-κB(p65)and phosphorylated MAPK signaling pathways.(3)Animal experiments showed that auranofin promoted wound healing in db/db diabetic mice,suggesting that auranofin has strong anti-inflammatory effects and may facilitate the healing of wounds in diabetic mice.
