上睑下垂
纳米载体
肺
材料科学
肺水肿
败血症
癌症研究
炎症
细胞内
药理学
炎症反应
氧化应激
肺泡巨噬细胞
细胞因子
巨噬细胞
促炎细胞因子
纳米技术
医学
细胞生物学
水肿
生物物理学
纳米结构
治疗效果
细胞毒性
DNA损伤
急性损伤
纳米毒理学
免疫学
作者
Yunlong Zhang,Mingliang Pan,Fei Ma,Changting He,Qin Gu,Yongli Wang,Zhou Pan,Huijuan Wang,Yan Yan,Xinting Fu,Yue Jia,Han Duan,Yanqiu Wu,Zihui Wei,Jiamei Wang,Bo Li,Yuhui Liao,Liying Zhan
标识
DOI:10.1021/acsami.6c01459
摘要
Sepsis-induced acute lung injury (SI-ALI) is a critical complication of sepsis characterized by severe pulmonary edema, hyper-inflammatory responses, and high mortality rates, for which precise therapeutic strategies remain limited. In this study, we developed a macrophage-targeting, dimethyl fumarate (DMF)-loaded tetrahedral DNA nanoplatform (T-D@TDN) and evaluated its physicochemical properties, antipyroptotic mechanisms, and therapeutic efficacy in SI-ALI. The nanostructure exhibits excellent biocompatibility, efficient alveolar macrophage (AM) targeting, and prolonged pulmonary retention following intranasal administration. In a murine model of SI-ALI induced by cecal ligation and puncture (CLP), T-D@TDN treatment significantly reduced pulmonary inflammatory cytokine levels and alleviated pulmonary edema and tissue injury, accompanied by a marked improvement in the 48-h survival rate. Mechanistically, T-D@TDN integrates a triple-regulation strategy to suppress pyroptosis: the TDN framework exerts intrinsic ROS-scavenging activity, while the released DMF activates the NRF2/HO-1 axis to further eliminate intracellular ROS and directly inhibits GSDMD cleavage. Collectively, these findings demonstrate that T-D@TDN functions as a multifunctional inhalable nanotherapeutic agent capable of multidimensionally regulating oxidative stress and pyroptosis pathways, providing a promising noninvasive strategy for the treatment of SI-ALI and related inflammatory lung diseases.
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