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紫甘薯来源的碳点作为一种有前景的抗炎生物材料,用于减轻巨噬细胞中脂多糖诱导的炎症。

Carbon dots from purple sweet potato as a promising anti-inflammatory biomaterial for alleviating the LPS-induced inflammation in macrophages.

作者信息

Jiang Jiebang, Pan Zhiyuan, Su Yiren, Dai Lu, Xu Nana, Wu Han, Chen Xin

机构信息

Department of General Surgery, Affiliated Hospital of Nantong University, No.20 Xisi Road, Nantong, Jiangsu, 226001, China.

School of Life Sciences, Jiangsu Normal University, Xuzhou, Jiangsu, 221116, China.

出版信息

J Nanobiotechnology. 2025 May 30;23(1):397. doi: 10.1186/s12951-025-03494-9.

Abstract

This study synthesizes carbon dots derived from crude extracts of purple sweet potato (CPP-CDs) and evaluates its anti-inflammatory effects in a lipopolysaccharide (LPS) -induced acute inflammation model. Characterization revealed that CPP-CDs possess a uniform spherical structure and excellent photoluminescent properties. In vitro, CPP-CDs significantly inhibited the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), reduced the accumulation of reactive oxygen species (ROS), suppressed pyroptosis, and facilitated the polarization of macrophages from the M1 phenotype to the M2 phenotype. In vivo, CPP-CDs significantly improved the survival rates of LPS-treated mice, mitigated tissue damage, and suppressed the levels of pro-inflammatory cytokines. Mechanistic studies indicated that CPP-CDs exert anti-inflammatory effects through the inhibition of the TLR4/NF-κB signaling pathway and the modulation of the NLRP3 inflammasome. Additionally, CPP-CDs exhibited excellent biocompatibility, with no significant toxicity observed in mice. This study provides strong evidence supporting the application of CPP-CDs as a novel anti-inflammatory material, highlighting their potential for acute inflammation treatment and expanding the possibilities for the development of carbon-dot-based anti-inflammatory therapies.

摘要

本研究合成了源自紫薯粗提物的碳点(CPP-CDs),并在脂多糖(LPS)诱导的急性炎症模型中评估了其抗炎作用。表征显示CPP-CDs具有均匀的球形结构和优异的光致发光特性。在体外,CPP-CDs显著抑制促炎细胞因子(IL-1β、IL-6、TNF-α)的表达,减少活性氧(ROS)的积累,抑制细胞焦亡,并促进巨噬细胞从M1表型向M2表型极化。在体内,CPP-CDs显著提高LPS处理小鼠的存活率,减轻组织损伤,并抑制促炎细胞因子水平。机制研究表明,CPP-CDs通过抑制TLR4/NF-κB信号通路和调节NLRP3炎性小体发挥抗炎作用。此外,CPP-CDs表现出优异的生物相容性,在小鼠中未观察到明显毒性。本研究为CPP-CDs作为新型抗炎材料的应用提供了有力证据,突出了其在急性炎症治疗中的潜力,并拓展了基于碳点的抗炎疗法的发展可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7994/12124011/20e16a575831/12951_2025_3494_Sch1_HTML.jpg

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