糖纳米颗粒中的 SDF-1α 表现出完全的活性，并降低了大鼠的肺动脉高压。
SDF-1α in glycan nanoparticles exhibits full activity and reduces pulmonary hypertension in rats.
机构信息
Department of Medicine, Brigham and Women's Hospital and Harvard Medical School , Boston, Massachusetts 02115, United States.
出版信息
Biomacromolecules. 2013 Nov 11;14(11):4009-20. doi: 10.1021/bm401122q. Epub 2013 Oct 18.
Abstract
To establish a homing signal in the lung to recruit circulating stem cells for tissue repair, we formulated a nanoparticle, SDF-1α NP, by complexing SDF-1α with dextran sulfate and chitosan. The data show that SDF-1α was barely released from the nanoparticles over an extended period of time in vitro (3% in 7 days at 37 °C); however, incorporated SDF-1α exhibited full chemotactic activity and receptor activation compared to its free form. The nanoparticles were not endocytosed after incubation with Jurkat cells. When aerosolized into the lungs of rats, SDF-1α NP displayed a greater retention time compared to free SDF-1α (64 vs 2% remaining at 16 h). In a rat model of monocrotaline-induced lung injury, SDF-1α NP, but not free form SDF-1α, was found to reduce pulmonary hypertension. These data suggest that the nanoparticle formulation protected SDF-1α from rapid clearance in the lung and sustained its biological function in vivo.
摘要
为了在肺部建立归巢信号，以招募循环干细胞进行组织修复，我们通过将 SDF-1α 与葡聚糖硫酸盐和壳聚糖复合，制备了一种纳米颗粒 SDF-1α NP。数据显示，SDF-1α 在体外长时间内（37°C 下 7 天内 3%）几乎不会从纳米颗粒中释放出来；然而，与游离形式相比，掺入的 SDF-1α 表现出完全的趋化活性和受体激活。Jurkat 细胞孵育后，纳米颗粒不会被内吞。当雾化到大鼠肺部时，SDF-1α NP 与游离 SDF-1α 相比，显示出更长的保留时间（16 小时时分别为 64%和 2%）。在野百合碱诱导的肺损伤大鼠模型中，SDF-1α NP 可降低肺动脉高压，而游离形式的 SDF-1α 则没有这种作用。这些数据表明，纳米颗粒制剂可防止 SDF-1α 在肺部快速清除，并在体内维持其生物学功能。
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