Abstract
The aim of this work was the development of microstructured lipid carriers (MLC) based on chitosan (CH) and containing N-acetylcysteine (NAC), a mucolytic and antioxidant agent, to inhibit the formation of Pseudomonas aeruginosa biofilm. MLC were prepared using the high shear homogenization technique. The MLC were characterized for morphology, particle size, Z potential, encapsulation efficiency and drug release. The antioxidant properties of NAC-loaded microstructured carriers were evaluated through an in vitro spectrophotometer assay. Finally, the activity of NAC-CH-MLC on biofilm production by Pseudomonas aeruginosa was also evaluated. Results obtained from this study highlighted that the use of chitosan into the inner aqueous phase permitted to obtain microstructured particles with a narrow size range and with good encapsulation efficiency. NAC-loaded MLC showed higher antioxidant activity than the free molecule, demonstrating how encapsulation increases the antioxidant effect of the molecule. Furthermore, the reduction of biofilm growth resulted extremely high with MLC being 64.74% ± 6.2% and 83.74% ± 9.95%, respectively, at 0.5 mg/mL and 2 mg/mL. In conclusion, this work represents a favorable technological strategy against diseases in which bacterial biofilm is relevant, such as cystic fibrosis.
Highlights
Cystic fibrosis (CF) is a genetic disorder caused by mutations of a gene encoding a multifunctional protein, the cystic fibrosis transmembrane regulator (CFTR), expressed on the apical membrane of epithelial cells and submucosal glands [1]
The microstructured lipid carriers (MLC) surface appeared smooth and no drug crystals were on the surface
Results highlighted that a concentration of 0.5 mg/mL of active compound on NAC-CH (MLC); chitosan (CH-MLC) produced a reduction of 64.74% ± 6.2% of P. aeruginosa biofilm growth, while the same amount of placebo MLC (CH-MLC_3) produced a reduction of only 8.57% ± 1.2% (p < 0.05)
Summary
Cystic fibrosis (CF) is a genetic disorder caused by mutations of a gene encoding a multifunctional protein, the cystic fibrosis transmembrane regulator (CFTR), expressed on the apical membrane of epithelial cells and submucosal glands [1].CTFR represents a 1480 residue-long membrane protein, component of the ATPbinding cassette (ABC) transporter family and it functions as an ion channel; the presence of a supplementary regulatory region and N- and C-terminal extensions constituted by 80 and 30 residues in length, respectively, are a distinctive feature of this protein [2]. Cystic fibrosis (CF) is a genetic disorder caused by mutations of a gene encoding a multifunctional protein, the cystic fibrosis transmembrane regulator (CFTR), expressed on the apical membrane of epithelial cells and submucosal glands [1]. The loss of ion conductance across the membrane of these cells produces impaired ion and liquid homeostasis, causing a multiorgan disorder [3]; the organs mainly affected are the lungs, pancreas, liver, gut and the reproductive system (especially in males, due to the obstruction of the spermatic ducts) [2]. CF is the most frequent, and it is a cause of early mortality in Caucasians worldwide. This autosomal recessive inherited disease occurs in approximately
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