Synergistic effects of silver nanoparticles and cisplatin in combating inflammation and hyperplasia of airway stents.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34820570.
- Also identified by DOI 10.1016/j.bioactmat.2021.07.029 and PMC identifier 8586718.
- Licence recorded as CC BY-NC-ND.
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Abstract
Anti-inflammatory and antihyperplasia activities are essential requirements for the successful use of airway stents. In this work, silver nanoparticles (AgNPs) and cisplatin (DDP) were combined in a synergistic modification strategy to improve the surface function of airway stents. Using polycaprolactone (PCL) as a drug carrier, a dual-functional PCL-AgNPs-DDP fiber film-coated airway stent was fabricated by electrospinning. The physicochemical and biological properties of the obtained fiber films were examined. The ATR-FTIR, XPS, SEM-EDS and TEM results suggested that AgNPs and DDP could be successfully immobilized onto the airway stent surface. The drug release and surface degradation results revealed that AgNPs and DDP can undergo sustained release from films for 30 d, and the weight loss was approximately 50% after 35 d. In addition, the dual-functional fiber film suppressed human embryonic lung fibroblast growth and exhibited excellent antibacterial activity against <i>Staphylococcus aureus, Pseudomonas aeruginosa</i> and <i>Candida albicans</i>. Furthermore, the effectiveness of the dual-functional fiber film-coated airway stent was evaluated by application to the trachea of New Zealand rabbits. The <i>in vivo</i> results indicated that PCL-AgNPs-DDP fiber film-coated airway stent can significantly inhibit granulation tissue formation and collagen deposition, reduced the expression of IL-8, TNF-α, IL-1α, PCNA, α-SMA and CD68, and ultimately achieved anti-inflammatory and antihyperplasia effects. Hence, this study provides a dual-functional surface-coated airway stent to address the clinical complications associated with respiratory tract inflammation and granulation tissue hyperplasia, thus inhibiting tracheal stenosis.