Inhibiting the vascular smooth muscle cells proliferation by EPC and DPPC liposomes encapsulated magnolol

Percutaneous transluminal coronary angioplasty (PTCA) is a non-srugical modality for treating stennosis. However, the recurrence of restenosis in 30-50% patients within 6 months is the major drawback of PTCA. The major reason of restenosis is the proliferation of the vascular smooth muscle cells (VSMCs). Magnolol, a pure compound extracted from Magnolia officianalis, encapsulated by liposome was investigated for inhibiting the VSMCs proliferation leading to restenosis by PTCA. 1,2-Diacyl-Sn-glycero-3-phosphocholine (EPC) and 1,2-dipalmitoyl-Sn-glycerol-3-phosphocholine (DPPC) liposomes were utilized to encapsulate the magnolol. EPC liposome obtained the higher encapsulation efficiency than DPPc liposomes from Uv-vis spectroscopy study. The inhibiting efficiency of EPC and DPPc liposomes encapsulated magnolol was higher than pure magnolol. Magnolol encapsulated by EPC liposomes had better efficiency on inhibiting VSMCs than DPPC liposome. Addition of cholestrol in liposomes could slightly enhance the encapsulation efficiency. The particles sizer analysis revealed the average particles size of EPc and DPPC liposomes encapsulated magnolol became larger than pure EPC or DPPC liposomes. From the transmission electron microscopy (TEM) analysis, the magnolol seems to interfere with EPC and DPPc liposomes to form a homogeneous lipid bilayer. (c) 2008 Taiwan Institute of Chemical Engineers. Published by Elsevier B.V. All rights reserved.