Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin.

Curcumin is a widely known natural phytochemical from plant Curcuma longa. In recent years, curcumin has received increasing attention because of its capability to induce apoptosis and inhibit cell proliferation as well as its anti-inflammatory properties in different cancer cells. However, the therapeutic benefits of curcumin are severely hampered due to its particularly low absorption via trans-dermal or oral bioavailability. Phototherapy with visible light is gaining more and more support in dermatological therapy. Red light is part of the visible light spectrum, which is able to deeply penetrate the skin to about 6 mm, and directly affect the fibroblast of the skin dermis. Blue light is UV-free irradiation which is fit for treating chronic inflammation diseases. In this study, we show that curcumin at low concentrations (1.25-3.12 µM) has a strong anti-proliferative effect on TNF-α-induced psoriasis-like inflammation when applied in combination with light-emitting-diode devices. The treatment was especially effective when LED blue light at 405 nm was combined with red light at 630 or 660 nm, which markedly amplified the anti-proliferative and apoptosis-inducing effects of curcumin. The experimental results demonstrated that this treatment reduced the viability of human skin keratinocytes, decreased cell proliferation, induced apoptosis, inhibited NF-κB activity and activated caspase-8 and caspase-9 while preserving the cell membrane integrity. Moreover, the combined treatment also down-regulated the phosphorylation level of Akt and ERK. Taken together, our results indicated that the combination of curcumin with LED blue light united red light irradiation can attain a higher efficiency of regulating proliferation and apoptosis in skin keratinocytes.

Quantum dots encapsulated glycopolymer vesicles: synthesis, lectin recognition and photoluminescent properties.

Biomimetic star-shaped glycopolymer poly(ɛ-caprolactone)-b-poly(2-aminoethyl methacrylate-b-poly(gluconamidoethylmethacrylate) (SPCL-PAMA-PGAMA) was synthesized by the combination of ring opening polymerization (ROP) and reversible addition-fragmentation chain transfer (RAFT) polymerization. The glycopolymer self-assembled into vesicles with low critical aggregation concentration (CAC) (0.0075 mg/mL). Then, the carboxylic capped CdTe QDs were encapsulated within the glycopolymer vesicles. The QDs encapsulated glycopolymer vesicles (Gly@QDs vesicles) could specifically bind Concanavalin A (Con A) without changing the photoluminescent properties of the Gly@QDs vesicles. Cell viability studies revealed that the cytotoxicity of the Gly@QDs vesicles was remarkably improved as compared to that of the original QDs. The Gly@QDs vesicles were internalized by Hep G2 cells and then emitted green fluorescence in the cells. Consequently, these Gly@QDs vesicles provided a multifunctional platform for targeted delivery and imaging.

Biomimetic glycopolymers tethered gold nanoparticles: preparation, self-assembly and lectin recognition properties.

Biomimetic glycopolymers poly(gluconamidoethylmethacrylate)-b-poly(ɛ-caprolactone)-b-poly(gluconamidoethylmethacrylate) with degradable disulfide groups in the backbone (PGAMA-PCL-SS-PCL-PGAMA) were synthesized by the combination of ring opening polymerization (ROP) and atom transfer radical polymerization (ATRP). The internal disulfide bonds were cleaved by reduction with dl-dithiothreitol to yield the corresponding thiol terminated glycopolymers. The thiol terminated glycopolymers were effectively anchored on the surface of gold nanoparticles to prepare the biomimetic glycopolymers modified gold nanoparticles (Gly@Au NPs). Moreover, the properties of the Gly@Au NPs in aqueous solution were investigated. Transmission electron microscopy (TEM) analysis revealed that the self-assembly morphology of the Gly@Au NPs can be fine-tuned, from irregular clusters to spherical aggregates, by changing the weight fraction of the hydrophobic PCL block. Furthermore, the Gly@Au NPs had specific recognition with Concanavalin A (Con A).

Red light interferes in UVA-induced photoaging of human skin fibroblast cells.

The possible regulation mechanism of red light was determined to discover how to retard UVA-induced skin photoaging. Human skin fibroblasts were cultured and irradiated with different doses of UVA, thus creating a photoaging model. Fibroblasts were also exposed to a subtoxic dose of UVA combined with a red light-emitting diode (LED) for five continuous days. Three groups were examined: control, UVA and UVA plus red light. Cumulative exposure doses of UVA were 25 J cm(-2), and the total doses of red light were 0.18 J cm(-2). Various indicators were measured before and after irradiation, including cell morphology, viability, ß-galactosidase staining, apoptosis, cycle phase, the length of telomeres and the protein levels of photoaging-related genes. Red light irradiation retarded the cumulative low-dose UVA irradiation-induced skin photoaging, decreased the expression of senescence-associated ß-galactosidase, upregulated SIRT1 expression, decreased matrix metalloproteinase MMP-1 and the acetylation of p53 expression, reduced the horizon of cell apoptosis and enhanced cell viability. Furthermore, the telomeres in UVA-treated cells were shortened compared to those of cells in the red light groups. These results suggest that red light plays a key role in the antiphotoaging of human skin fibroblasts by acting on different signaling transduction pathways.