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BACKGROUND

Acute lung injury (ALI) triggers the activation of pulmonary macrophages, which in turn produce excessive amounts of reactive oxygen species (ROS).

RESULTS

We synthesized ROS-responsive red light-emitting carbon dots (RCMNs) that target lung macrophages, possess bioimaging capabilities, and efficiently eliminate intracellular ROS, thereby demonstrating anti-inflammatory effects for treating acute lung injury (ALI). In an LPS-induced ALI mouse model, RCMNs showed bioimaging and therapeutic potential, reducing lung damage and inflammation by targeting ROS-damaged tissue. RCMNs also improved alveolar macrophage activity, decreased inflammatory cytokines (TNF-α and IL-6), and enhanced survival in endotoxic shock, indicating their therapeutic potential for ALI. RNA-seq analysis revealed that RCMNs modulate signaling pathways related to calcium, TNF, and Toll-like receptors, highlighting their role in regulating inflammation and immune responses. Mechanistically, RCMNs alleviate inflammation in ALI by enhancing mitochondrial function in lung macrophages, as evidenced by improved mitochondrial morphology and membrane potential.

CONCLUSIONS

This protective effect is mediated through the regulation of intracellular Ca levels and mitochondrial respiratory chain complexes, suggesting RCMNs as a therapeutic strategy for mitochondrial dysfunction in ALI.

BACKGROUND

Acute lung injury (ALI) triggers the activation of pulmonary macrophages, which in turn produce excessive amounts of reactive oxygen species (ROS).

RESULTS

CONCLUSIONS

背景

急性肺损伤（ALI）会触发肺巨噬细胞的激活，进而产生过量的活性氧（ROS）。

结果

我们合成了针对肺巨噬细胞的 ROS 响应性红色发光碳点（RCMNs），它们具有生物成像功能，并且能够有效消除细胞内的 ROS，从而表现出治疗急性肺损伤（ALI）的抗炎作用。在 LPS 诱导的 ALI 小鼠模型中，RCMNs 显示出生物成像和治疗潜力，通过靶向 ROS 损伤组织来减轻肺损伤和炎症。RCMNs 还能提高肺泡巨噬细胞的活性，降低炎症细胞因子（TNF-α和 IL-6）的水平，并提高内毒素休克的存活率，表明其在 ALI 治疗方面的潜力。RNA-seq 分析显示，RCMNs 调节与钙、TNF 和 Toll 样受体相关的信号通路，突出了它们在调节炎症和免疫反应中的作用。从机制上讲，RCMNs 通过增强肺巨噬细胞中线粒体功能来减轻 ALI 中的炎症，这表现在改善的线粒体形态和膜电位上。