Qin Xianyan, Zhang Luhan, Miao Yang-Bao, Jiang Linxi, Zou Liang, Wang Qin, Shi Yi
Sichuan Provincial Key Laboratory for Human Disease Gene Study and the Center for Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
School of Food and Biological Engineering, Chengdu University, Chengdu, Sichuan, 610106, China.
J Nanobiotechnology. 2024 Dec 18;22(1):755. doi: 10.1186/s12951-024-03061-8.
Rheumatoid arthritis (RA) is an autoimmune disorder characterized by painful swelling and inflammation, arising from the immune system attacking on healthy cells. However, arthritic sites often experience increased lymph flow, hastening drug clearance and potentially reducing treatment effectiveness. To address this challenge, an in situ size amplification has been proposed to reduce lymphatic clearance and thereby enhance arthritis therapy. This system has been developed based on a conjugate of dexamethasone (Dex) and polysialic acid (PSA), linked via an acid-sensitive linker, supplemented with bis-5-hydroxytryptamine (Bis-5HT) on the PSA backbone. Under physiological conditions, the system autonomously assembles into stable nanoparticles (PD5NPs), facilitating prolonged circulation and targeted delivery to inflamed joints. Upon arrival at arthritic joints, Bis-5HT reacts to elevated myeloperoxidase (MPO) levels and oxidative stress, prompting particle aggregation and in-situ size amplification. This in situ size amplification nanocarrier effectively reduces lymphatic clearance and serves as reservoirs for sustained Dex release in acidic pH environments within arthritic sites, thus continuously alleviating RA symptoms. Moreover, investigation on the underlying mechanism elucidates how the in situ size amplification nanocarrier influences the transportation of PD5NPs from inflamed joints to lymphatic vessels. Our study offers valuable insights for optimizing nanomedicine performance in vivo and augmenting therapeutic efficacy.
类风湿性关节炎(RA)是一种自身免疫性疾病,其特征为疼痛性肿胀和炎症,由免疫系统攻击健康细胞引起。然而,关节炎部位的淋巴液流动通常会增加,加速药物清除并可能降低治疗效果。为应对这一挑战,有人提出进行原位尺寸放大以减少淋巴清除,从而增强关节炎治疗效果。该系统是基于地塞米松(Dex)与聚唾液酸(PSA)的共轭物开发的,二者通过酸敏连接子相连,并在PSA主链上补充了双5-羟色胺(Bis-5HT)。在生理条件下,该系统自动组装成稳定的纳米颗粒(PD5NP),有助于延长循环时间并靶向递送至发炎关节。到达关节炎关节后,Bis-5HT对升高的髓过氧化物酶(MPO)水平和氧化应激作出反应,促使颗粒聚集并原位尺寸放大。这种原位尺寸放大纳米载体有效地减少了淋巴清除,并在关节炎部位的酸性pH环境中作为地塞米松持续释放的储存库,从而持续缓解类风湿性关节炎症状。此外,对潜在机制的研究阐明了原位尺寸放大纳米载体如何影响PD5NP从发炎关节向淋巴管的转运。我们的研究为优化体内纳米药物性能和提高治疗效果提供了有价值的见解。