Study summary · research use only
Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse study, researchers loaded the tripeptide lysine-proline-valine (KPV) into hyaluronic acid (HA)-functionalized polymeric nanoparticles (NPs) to treat ulcerative colitis (UC). The resulting HA-KPV-NPs had a particle size of about 272.3 nm and a zeta potential of about -5.3 mV, and were reported to target delivery of KPV to colonic epithelial cells and macrophages while appearing nontoxic and biocompatible with intestinal cells. HA-KPV-NPs were reported to act against UC by promoting mucosal healing and reducing inflammation. Oral administration of HA-KPV-NPs encapsulated in a chitosan/alginate hydrogel was reported to reduce mucosa damage and TNF-alpha more than a KPV-NP/hydrogel system in a mouse model, and the authors describe the system as enabling KPV to reach colonic lumen and colitis tissue.
Abstract
Overcoming adverse effects and selectively delivering drug to target cells are two major challenges in the treatment of ulcerative colitis (UC). Lysine-proline-valine (KPV), a naturally occurring tripeptide, has been shown to attenuate the inflammatory responses of colonic cells. Here, we loaded KPV into hyaluronic acid (HA)-functionalized polymeric nanoparticles (NPs). The resultant HA-KPV-NPs had a desirable particle size (∼272.3 nm) and a slightly negative zeta potential (∼-5.3 mV). These NPs successfully mediated the targeted delivery of KPV to key UC therapy-related cells (colonic epithelial cells and macrophages). In addition, these KPV-loaded NPs appear to be nontoxic and biocompatible with intestinal cells. Intriguingly, we found that HA-KPV-NPs exert combined effects against UC by both accelerating mucosal healing and alleviating inflammation. Oral administration of HA-KPV-NPs encapsulated in a hydrogel (chitosan/alginate) exhibited a much stronger capacity to prevent mucosa damage and downregulate TNF-α, thus they showed a much better therapeutic efficacy against UC in a mouse model, compared with a KPV-NP/hydrogel system. These results collectively demonstrate that our HA-KPV-NP/hydrogel system has the capacity to release HA-KPV-NPs in the colonic lumen and that these NPs subsequently penetrate into colitis tissues and enable KPV to be internalized into target cells, thereby alleviating UC.
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