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通过抑制免疫细胞浸润并有效递送糖皮质激素来增强多发性硬化症治疗的炎症靶向仿生纳米诱饵

Inflammation-Targeted Biomimetic Nano-Decoys via Inhibiting the Infiltration of Immune Cells and Effectively Delivering Glucocorticoids for Enhanced Multiple Sclerosis Treatment.

作者信息

Yang Yiling, Zhao Yuzhen, Liu Huixian, Wu Xinyun, Guo Mingming, Xie Li, Wang Guangsheng, Shi Jinjin, Yu Wenyan, Dong Gang

机构信息

Department of Ultrasound, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.

School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.

出版信息

Adv Healthc Mater. 2025 Jan;14(2):e2402965. doi: 10.1002/adhm.202402965. Epub 2024 Oct 23.

DOI:10.1002/adhm.202402965
PMID:39440626
Abstract

Excessive infiltration of neutrophil and inflammatory cytokines accumulation as well as the inadequate delivery of drugs to the targeted site are key pathological cascades in multiple sclerosis (MS). Herein, inflammation-targeting biomimetic nano-decoys (TFMN) is developed that inhibit the infiltration of immune cells and effectively deliver glucocorticoids to lesions for enhanced MS treatment. Nano-decoys encapsulated with the glucocorticoid methylprednisolone (MPS) are prepared by coating neutrophil membrane (NM) on nanoparticles formed by the self-assembly of tannic acid and poloxamer188/pluronic68. Benefiting from the natural inflammation-targeting ability of activated neutrophil membranes, TFMN can target the lesion site and prevent neutrophils infiltration by adsorbing and neutralizing elevated neutrophil-related cytokines, subsequently modulating the inflammatory microenvironment in experimental autoimmune encephalomyelitis mice. TFMN exhibits a strong antioxidant capacity and scavenged excessive reactive oxygen species to enhance neuronal protection. Furthermore, at the inflammation site, perforin, discharged by cytotoxic T-lymphocytes, triggered the controlled release of MPS within the TFMN through perforin-formed pores in the NM. Simultaneously, this mechanism protected neurons from perforin-induced toxicity. The MPS liberated at the targeted site achieves optimal drug accumulation, thereby enhancing therapeutic efficacy. In conclusion, the innovative system shows potential for integrating various therapeutic agents, offering a novel strategy for CNS disorders.

摘要

中性粒细胞过度浸润、炎性细胞因子蓄积以及药物向靶位点递送不足是多发性硬化症(MS)的关键病理级联反应。在此,开发了一种靶向炎症的仿生纳米诱饵(TFMN),其可抑制免疫细胞浸润,并有效将糖皮质激素递送至病灶以增强MS治疗效果。通过将中性粒细胞膜(NM)包覆在由单宁酸与泊洛沙姆188/普朗尼克68自组装形成的纳米颗粒上,制备了包载糖皮质激素甲泼尼龙(MPS)的纳米诱饵。得益于活化中性粒细胞膜天然的炎症靶向能力,TFMN可靶向病灶部位,通过吸附和中和升高的中性粒细胞相关细胞因子来阻止中性粒细胞浸润,随后调节实验性自身免疫性脑脊髓炎小鼠的炎症微环境。TFMN具有强大的抗氧化能力,可清除过量的活性氧以增强神经元保护作用。此外,在炎症部位,细胞毒性T淋巴细胞释放的穿孔素通过在NM中形成的穿孔素孔触发TFMN内MPS的控释。同时,该机制保护神经元免受穿孔素诱导的毒性。在靶位点释放的MPS实现了最佳的药物蓄积,从而提高了治疗效果。总之,该创新系统显示出整合多种治疗剂的潜力,为中枢神经系统疾病提供了一种新策略。

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