BACKGROUND: Ultraviolet-B (UVB) radiation is the leading environmental cause of skin damage and photoaging. The epidermis and dermis layers of the skin mainly absorb UVB. UVB stimulates apoptosis, cell cycle arrest, generation of reactive oxygen species, and degradation of collagen and elastin fibers.
OBJECTIVE: This study investigated the potential of human growth hormone (hGH) in protecting the skin fibroblasts and keratinocytes (HFFF-2 and HaCaT cell lines) from UVB-induced damage.
METHODS: The MTT assay was performed to evaluate UVB-induced mitochondrial damage via assessing the mitochondrial dehydrogenase activity, and flow cytometry was carried out to investigate the effects of UVB and hGH on the cell cycle and apoptosis of UVB-irradiated cells. In addition, the fold change mRNA expression levels of Type I collagen and elastin in HFFF-2 cells were evaluated using the qRT-PCR method following UVB exposure.
RESULTS: We observed that treatment of cells with hGH before UVB exposure inhibited UVB-induced loss of mitochondrial dehydrogenase activity, apoptosis, and sub-G1 population formation in both cell lines. We also found that hGH-treated HFFF-2 cells showed up-regulated mRNA expression of Type I collagen, elastin, and IGF-1 in response to UVB irradiation.
CONCLUSIONS: These findings suggest hGH as a potential anti-UVB compound that can protect skin cells from UVB-induced damage. Our findings merit further investigation and can be used to better understand the role of hGH in skin photoaging.

The purpose of this study was to isolate exopolysaccharides (EPS) from lactic acid bacteria (LAB) and evaluate EPS anti-UVB viability. Lacticaseibacillus rhamnosus VHPriobi O17 with high EPS production was screened from 34 strains of LAB. The EPS (OP-2) produced by L. rhamnosus VHPriobi O17 was purified by alcohol precipitation and DEAE-μSphere anion exchange chromatography. By ion chromatography, FT-IR spectrum and gel column chromatography, EPS (OP-2) was a novel Man-like polysaccharide with the weight-averaged molecular of 84.2 kDa. The EPS (OP-2) can effectively alleviate HaCaT cells apoptosis and overproduction of reactive oxygen species (ROS) induced by UVB. The results also showed that it inhibited the release of pro-inflammatory cytokines (IL-1α, IL-6 and IL-8); and suppressed the phosphorylation cascade of JNK and p38 MAPK to reduce the expression level of active-caspase3, ultimately prevented cell apoptosis. Thus, the EPS produced by L. rhamnosus VHPriobi O17 have the potential to be used for human anti-UVB irradiation.

Ultraviolet (UV) radiation has deleterious effects on cells through direct damage to DNA or through increasing generation of reactive oxygen species (ROS). The flavonol quercetin (Qu) provides cellular protection against UV radiation and the current investigation was carried out to develop a deformable liposome formulation of Qu to enhance its delivery into human skin and to improve its anti-UVB effect. The influence of surfactants (including Span 20, Tween 80 and sodium cholate) on the properties of Qu deformable liposomes was investigated. Liposomes composed of Qu, phosphatidylcholine (PC), cholesterol (Chol), and Tween 80 showed high entrapment efficiencies (80.41±4.22%), small particle sizes (132±14nm), high elasticity (10.48±0.71), and prolonged drug release. The cell viability in UVB-irradiated HaCaT cells increased to 89.89±4.5% at 24h and 78.8±3.19% at 48h following treatment with Qu defomable liposomes. The ROS and malondialdehyde (MDA) level were also reduced. The penetration rate was 3.8-fold greater than that of the Qu suspension. Moreover, the edema and inflammation was alleviated by Qu deformable liposomes. These results showed the potential of deformable liposomes to enhance the anti-UVB effects of Qu both in vitro and in vivo.