Magnolol encapsulated by different acyl chain length of liposomes on inhibiting proliferation of smooth muscle cells

The pathological mechanism of percutaneous transluminal coronary angioplasty (PTCA) induced restenosis has been attributed to outgrowth of vascular smooth muscle cells. In this study, the inhibitions of magnolol encapsulated by liposome were better than pure 0.075 mg/mL magnolol. The MTT assay showed that the inhibition efficacy of these liposomes as a drug carrier had been reduced by increasing the fatty acyl chain length of phospholipids. From the transmission electron microscopy (TEM) analysis, the magnolol interfere the liposomes to form a homogeneous lipid bilayer. Of all tested liposomes, the smallest mean size distribution was found for DMPC (25.27 nm) that also had the best inhibitory effect on smooth muscle cells. The encapsulation efficiency that investigated by UV–vis spectroscopy showed DSPC > DPPC > DMPC. In the monolayer study, the fluorescence microscopy (FM) images showed that the pronounced domain formation was associated with a longer relaxation time of the collapse DSPC, DPPC, and DMPC monolayers and the lipid with longer acyl chain appeared to form a rigid monolayer.