Hydroxytyrosol mediates S100A9/TLR4/NF-κB signaling pathway to regulate macrophage polarization and improve wound healing in burn rats
10.13431/j.cnki.immunol.j.20250012
- VernacularTitle:羟基酪醇介导S100A9/TLR4/NF-κB信号通路调节巨噬细胞极化改善烧伤大鼠创面愈合
- Author:
Futai CHEN
1
;
Yongsuo LIU
;
Yuanzheng CHEN
Author Information
1. 261042 潍坊,山东第二医科大学附属医院烧伤整形外科;261042 潍坊,山东第二医科大学临床医学院
- Publication Type:Journal Article
- Keywords:
Burn;
Wound healing;
Hydroxytyrosol;
Macrophage polarization
- From:
Immunological Journal
2025;41(2):86-90,96
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of hydroxytyrosol-mediated macrophage polarization on burn wound healing in rats.Methods SD rats were randomly divided into burn group,hydroxytyrosol group,hydroxytyrosol+ov-NC group and hydroxytyrosol+ov-S100A9 group,with 10 rats in each group.Burn model was established by metal weight burn method.Wound healing rate was calculated;HE staining was used to observe the pathological changes of wound skin tissue in rats;immunofluorescence was used to detect the ratios of M1 and M2 macrophages in the wound skin of rats;ELISA was used to detect the levels of macrophage inflammatory factors in the wound skin of rats;Western blot was used to detect the expression of S100A9/TLR4/NF-κB signal pathway in wound skin of rats.Results Compared with the burn group,hydroxytyrosol group and hydroxytyrosol+ov-NC group demonstrated higher wound healing ability and alleviated pathological damage,lower levels of M1 type macrophages and related factors,higher levels of M2 type macrophages and related factors,and lower expression of S100A9,TLR4 and p-NF-κB p65 proteins.Compared with hydroxytyrosol group and hydroxytyrosol+ov-NC group,S100A9 overexpression reduced the wound healing ability and aggravated the pathological damage,increased M1 type macrophages and related factors,decreased M2 type macrophages and related factors,and increased the expression of S100A9,TLR4 and p-NF-κB p65 proteins in hydroxytyrosol+ov-S100A9 group.Conclusion Hydroxytyrosol promotes wound healing in burn rats by down-regulating S100A9,and its mechanism may be related to inhibiting the activation of TLR4/NF-κB signaling pathway and improving the imbalance of M1/M2 macrophages.
