Intra-articular (IA) drug delivery to treat osteoarthritis (OA) is limited by the short retention time of drugs in the joints due to poor specific targeting and non-responsiveness under acidic environment. A cartilage-targeting peptide was engineered to the surface of ferritin nanocages (CT-Fn) and loaded with an anti-inflammatory drug, metformin (Met), via the self-assembling nature of Fn nanocages. It demonstrated that the CT-Fn/Met could specifically bind to type II collagen, leading to the downregulation of catabolic markers of OA and promotion of cartilage-specific makers in IL-1β-induced chondrocytes. IA delivery of CT-Fn/Met prolonged the retention time for 3 weeks and remarkably reduced inflammation. Moreover, better release under acidic conditions which enabling longer retention time of Met after IA delivery in OA joints for one more week. CT-Fn/Met could target and efficiently enter chondrocytes, further inducing prolonged IA accumulation and achieving enhanced therapeutic efficacy for OA treatment.

由于在酸性环境下特异性靶向作用较弱和无反应性，关节内（IA）药物递送治疗骨关节炎（OA）的时间受到药物保留时间短的限制。将软骨靶向肽工程化到铁蛋白纳米笼（CT-Fn）的表面，并通过以下途径装载抗炎药二甲双胍（Met）：Fn纳米笼的自组装性质。结果表明，CT-Fn / Met可以特异性结合II型胶原，从而导致OA分解代谢标志物的下调并促进IL-1β诱导的软骨细胞中软骨特异性分子的生成。IA递送CT-Fn / Met可将保留时间延长3周，并显着减少炎症。而且，在酸性条件下更好的释放，使得IA关节在OA关节中递送后，Met的保留时间更长，可以持续一周以上。CT-Fn / Met可以靶向并有效进入软骨细胞，进一步诱导IA延长积累，并提高OA治疗的疗效。