The effective drug treatment of rheumatoid arthritis (RA) is hindered by poor delivery efficiency to the diseased site and the serious side effects caused by wide-spread drug distribution. Traditional drug-targeting strategies, such as ligand modification, are complex, laborious, and inefficient. Inspired by the intrinsic relationship between platelets and RA, platelet-mimetic nanoparticles (PNPs) were developed for targeted drug delivery in RA. Through platelet receptor-mediated adhesion, an intact platelet membrane was coated onto poly (lactic-co-glycolic acid) nanoparticles, endowing the resulting PNPs with various functional receptors. By coating with platelet membranes, the nanoparticles were stabilized and had a better circulation profile, providing a benefit for passive targeting. In vitro binding of PNPs to inflamed endothelium, and in vivo accumulation in joints of a collagen-induced arthritis (CIA) mouse model of RA were significantly improved via P-selectin and GVPI recognition, indicating that the PNPs could effectively target to RA tissues through multiple mechanisms, similar to natural platelets. Moreover, FK506, a model drug, was loaded into the PNPs and used to treat RA. Pharmacodynamic studies demonstrated that the FK506-PNPs had a notable anti-arthritic effect in CIA mice. This study provides a new biomimetic targeting strategy with great potential for the treatment of RA.

Although nanotechnology has been rapidly developed and applied in tumor targeting, the outcome of chemotherapy remains greatly restricted by the toxicity of cytotoxic drugs in normal tissues and cells. Therefore, the development of alternative delivery systems, with few side effects in normal cells, has attracted increasing attention. Energy restriction is a novel and promising approach to cancer treatment, which can restrict tumor growth via inhibition of cellular energy metabolism. In this study, a novel tumor targeting system, based on folate-conjugated bovine serum albumin (BSA), was developed to co-deliver albendazole and nanosilver simultaneously, to restrain the energy metabolism of tumor cells. This nanosystem showed stronger anti-tumor efficacy than those using nanoparticles without folic acid modification, nanosilver, or albendazole, both in vitro and in vivo. This nanosystem depleted cellular ATP via direct inhibition of glycolytic enzymes and mitochondrial damage, resulting in inhibition of proliferation, cell-cycle arrest, and apoptosis of tumor cells. The enhanced anti-tumor activity contributed to the tumor-targeting ability of this system, resulting in specific energy inhibition in tumor cells. Toxicity evaluation was performed to confirm the safety of this system. This nanosystem provides an efficient and safe strategy for tumor therapy.