Design and Evaluation of Paeonol-Loaded Liposomes in Thermoreversible Gels for Atopic Dermatitis

Abstract

Paeonol (PAE) is a hydrophobic drug. In this study, we encapsulated paeonol in a lipid bilayer of liposomes (PAE-L), which delayed drug release and increased drug solubility. When PAE-L was dispersed in gels (PAE-L-G) based on a poloxamer matrix material for local transdermal delivery, we observed amphiphilicity, reversible thermal responsiveness, and micellar self-assembly behavior. These gels can be used for atopic dermatitis (AD), an inflammatory skin disease, to change the surface temperature of the skin. In this study, we prepared PAE-L-G at an appropriate temperature for the treatment of AD. We then assessed the gel’s relevant physicochemical properties, in vitro cumulative drug release, and antioxidant properties. We found that PAE-loaded liposomes could be designed to increase the drug effect of thermoreversible gels. At 32 °C, PAE-L-G could change from solution state to gelatinous state at 31.70 ± 0.42 s, while the viscosity was 136.98 ± 0.78 MPa.S and the free radical scavenging rates on DPPH and H2O2 were 92.24 ± 5.57% and 92.12 ± 2.71%, respectively. Drug release across the extracorporeal dialysis membrane reached 41.76 ± 3.78%. In AD-like mice, PAE-L-G could also relieve skin damage by the 12th day. In summary, PAE-L-G could play an antioxidant role and relieve inflammation caused by oxidative stress in AD.

Therapeutic Potential of Hydrogel Based Sodium Alginate and Chitosan as A Multifunctional Drug Delivery System for Atopic Dermatitis

“…This release behavior was mainly due to T-Lip-AC not only passing through the lipid bilayer, but also through the three-dimensional network structure of ALG-CS. [40] The ultimate maximum release of T-AC in the first stage was due to its rapid release and adsorption onto the surface of ALG-CS, and the threedimensional network structure of ALG-CS extended the drug release time. The second stage, which extends from 24 h to 96 h, was achieved through a diffusion mechanism and resulted in prolonged drug release due to the slow dissolution and dispersion of the threedimensional network structure of the lipid core matrix and ALG-CS.…”