AI Article Synopsis
- The study investigates how a type of drug delivery system using nanoparticles containing the bisphosphonate alendronate can reduce neointimal formation in restenosis.
- The nanoparticles were found to effectively target macrophages, demonstrating significant cytotoxic effects in lab tests and leading to noteworthy reductions in artery narrowing in a rabbit model after balloon injury.
- Results indicate that the treatment not only decreased the amount of neointima but also correlated with lower levels of inflammatory markers, suggesting a mechanism where the nanoparticles temporarily reduce macrophage levels in the affected areas.
Article Abstract
Systemic transient depletion of monocytes and macrophages by liposome-encapsulated bisphosphonates (BPs), reduces neointimal formation in experimental restenosis. The aim of this study was to examine the antirestenotic effect of a polymeric nanoparticulate formulation containing the BP alendronate (ALN). The BP was successfully formulated in polylactide-co-glycolide (PLGA) nanoparticles (NP). ALN NP with negative charge, size of 223+/-64 nm, and high entrapment efficiency (55.1%) have been formulated. ALN NP exhibited a significant cytotoxic effect, in a dose-response relationship, on macrophage-like RAW264 cells in cell culture. Subcutaneously (SC) administrated ALN NP (1.5 mg/kg on days -1 and +6) resulted in a significant attenuation of neointima to media ratio (N/M) by 52.7% and stenosis by 39.7% 28 days after balloon injury in the hypercholesterolemic rabbit model. Moreover, a good correlation was found between macrophage abundance in the injured arteries and the extent of stenosis. ALN NP treatment resulted in the reduction of both interleukin-1beta and matrix metalloproteinases (2 and 9). It is concluded that a particulated dosage form of polymeric NP loaded with ALN reduce neointimal formation in vivo by systemic transient depletion of monocytes.
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| http://dx.doi.org/10.1016/j.jconrel.2006.03.010 | DOI Listing |
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