Neutrophil membrane-coated PLGA nanoparticles promoting the repair of myocardial ischemia-reperfusion injury in mice
10.12025/j.issn.1008-6358.2025.20250194
- VernacularTitle:中性粒细胞膜包覆的PLGA纳米粒促进小鼠心肌缺血再灌注损伤后修复
- Author:
Jing CHEN
1
;
Yanan SONG
1
;
Zheyong HUANG
1
;
Junbo GE
1
Author Information
1. Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, State Key Laboratory of Cardiology, National Clinical Research Center for Interventional Medicine, Shanghai Clinical Research Center for Interventional Medicine, Shanghai 200032, China.
- Publication Type:Originalarticle
- Keywords:
neutrophil membrane-coated nanoparticles;
myocardial ischemia-reperfusion;
inflammation neutralization;
tissue repair
- From:
Chinese Journal of Clinical Medicine
2025;32(3):384-391
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role and related mechanism of neutrophil membrane-coated poly(lactic-co-glycolic acid) (PLGA) nanoparticles (Neu-NP) in cardiac repair after acute myocardial ischemia-reperfusion (MI/R) injury in mice. Methods The male C57 mouse model of acute MI/R injury was established and randomly divided into three groups: PBS control group (injection of 200 μL PBS), NP treatment group (injection of 0.5 mg/mL NP 200 μL), and Neu-NP treatment group (injection of 0.5 mg/mL Neu-NP 200 μL). Neutrophil membranes were extracted and fused with PLGA nanoparticles to construct biomimetic Neu-NP. The in vivo homing ability of Neu-NP was assessed using ex vivo imaging technology in the MI/R injury model, and the expression levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the myocardium were measured using enzyme linked immunosorbent assay one day and three days after administration. Echocardiography was used to determine cardiac function indicators of MI/R injured mice 28 days post-administration. Immunofluorescence staining was used to observe angiogenesis repair and inflammatory cell infiltration in mouse heart tissue. Results Neu-NP, engineered by integrating neutrophil membranes with nanoparticles, inherited surface receptors (TNF-αR and IL-6R) and functioned as decoys for inflammatory targeting. Compared with the PBS control group and NP treatment group, the secretion levels of TNF-α and IL-6 in the damaged myocardium of the Neu-NP treatment group were significantly decreased one and three days after administration (P＜0.05); 28 days after administration, the cardiac ejection fraction in the Neu-NP treatment group was significantly higher than that in the other two groups (P＜0.05). Immunofluorescence staining indicated a significant increase in the proportion of angiogenesis in the myocardial infarction area and a significant reduction in inflammation cell infiltration (P＜0.05). Conclusions Neu-NP plays an important role in cardiac tissue repair after MI/R injury by alleviating inflammatory factors in the damaged area and promoting angiogenesis.
