Co-Encapsulation of EGCG and Quercetin in Liposomes for Optimum Antioxidant Activity.

Although different delivery systems have been developed to overcome the limits of Epigallocatechin-3-gallate (EGCG) and quercetin in food application, none have referred to their simultaneous encapsulation. In this study, these two polyphenols were successfully co-loaded into liposomes. Under the optimal conditions (lecithin-total polyphenols ratio 25:1, lecithin-cholesterol ratio 6:1, lecithin-Tween 80 ratio 8:1 and ultrasonic time 2 min), the mean size, polydispersity index (PDI) and zeta potential of liposomes were 111.10 ± 0.52 nm, 0.259 ± 0.006 and -19.83 ± 0.45 mV, with an encapsulation efficiency of 64.05 ± 1.56% and 61.73 ± 2.55% for EGCG and quercetin, respectively. After 30-day storage, an increase of 4.05% was observed in the mean size with no significant change (P ≥ 0.05) in the PDI and zeta potential. Moreover, 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay revealed a synergistic antioxidant effect of the two compounds in liposomal system. These results demonstrated that co-encapsulation of EGCG and quercetin enhances their effectiveness. PRACTICAL APPLICATION: EGCG and quercetin are natural polyphenols abound in the human diet with diverse biological activities. These two polyphenols were successfully co-encapsulated into a homogeneous and stable liposomal system. Interestingly, a synergistic antioxidant effect of the two polyphenols was observed due to co-encapsulation. This indicated that the simultaneous delivery of EGCG and quercetin was an attractive approach to improve their functionality for expanding their application in food, cosmetic and pharmaceutical industries.

Curcumin improves neural function after spinal cord injury by the joint inhibition of the intracellular and extracellular components of glial scar.

BACKGROUND: Spinal cord injury (SCI) is characterized by a high rate of disability and imposes a heavy burden on society and patients. SCI can activate glial cells and lead to swelling, hyperplasty, and reactive gliosis, which can severely reduce the space for nerve growth. Glial cells can secrete a large amount of extracellular inhibitory components, thus altering the microenvironment of axon growth. Both these factors seriously impede nerve regeneration. In the present study, we investigate whether curcumin (cur), a phytochemical compound with potent anti-inflammatory effect, plays a role in the repair of SCI. MATERIALS AND METHODS: We established a rat model of SCI and treated the animals with different concentrations of cur. Using behavioral assessment, immunohistochemistry, real-time polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay, we detected the intracellular and extracellular components of glial scar and related cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, nuclear factor (NF)-κb, transforming growth factor (TGF)-ß1, TGF-ß2, and sex determining region Y-box (SOX)-9. RESULTS: We found that cur inhibited the expression of proinflammatory cytokines, such as TNF-α, IL-1ß, and NF-κb; reduced the expression of the intracellular components glial fibrillary acidic protein through anti-inflammation; and suppressed the reactive gliosis. Also, cur inhibited the generation of TGF-ß1, TGF-ß2, and SOX-9; decreased the deposition of chondroitin sulfate proteoglycan by inhibiting the transforming growth factors and transcription factor; and improved the microenvironment for nerve growth. Through the joint inhibition of the intracellular and extracellular components of glial scar, cur significantly reduced glial scar volume and improved the Basso, Beattie, and Bresnahan locomotor rating and axon growth. CONCLUSIONS: Our data support a role for curcumin in promoting neural function recovery after SCI by the joint inhibition of the intracellular and extracellular components of glial scar, providing an important strategy for treating SCI.

NGR-based strategies for targeting delivery of chemotherapeutics to tumor vasculature.

In the last decades, NGR-containing peptides have been proved useful for ligand-directed targeted delivery of various chemotherapeutic drugs to tumor vasculature. Aminopeptidase N (APN; CD13) has been demonstrated to be a key binding site for NGR peptides on tumor vasculature. For drug targeting, chemical means have been applied to couple NGR-peptides to small molecule drugs, such as cytokines, antiangiogenic compounds, viral particles, contrast agents, DNA complexes and other biologic response modifiers. Some products have shown impressive results in preclinical animal models, such as NGR-TNF which was currently tested in Phase III trials. In this article we will review the process of NGR-to-isoDGR transition and provide suggestions for the design of the diverse NGR peptide-chemotherapeutics conjugates.