Photoprotective Effects of Cycloheterophyllin against UVA-Induced Damage and Oxidative Stress in Human Dermal Fibroblasts

Abstract

Ultraviolet (UV) radiation, particularly ultraviolet A (UVA), is known to play a major role in photoaging of the human skin. Many studies have demonstrated that UV exposure causes the skin cells to generate reactive oxygen species and activates the mitogen-activated protein kinase (MAPK) pathway. Previous studies have also demonstrated that cycloheterophyllin has an antioxidant effect and can effectively scavenge free radicals. Extending the aforementioned investigations, in this study, human dermal fibroblasts were used to investigate the protective effect of cycloheterophyllin against UV-induced damage. We found that cycloheterophyllin not only significantly increased cell viability, but also attenuated the phosphorylation of MAPK after UVA exposure. Furthermore, cycloheterophyllin could reduce hydrogen peroxide (H2O2) generation and down-regulate H2O2-induced MAPK phosphorylation. In the in vivo studies, the topical application of cycloheterophyllin before UVA irradiation significantly decreased trans-epidermal water loss (TEWL), erythema, and blood flow rate. These results indicate that cycloheterophyllin is a photoprotective agent that inhibits UVA-induced oxidative stress and damage, and could be used in the research on and prevention of skin photoaging.

The effect of Cyanidin-3-o-glucoside on UVA-induced damage in human dermal fibroblasts

“…In our study, C3G increased the low levels of p‐ERK induced by UVA. Huang et al and Hsu et al found that p‐P38 was significantly increased in HDFs after UVA irradiation, consistent with the findings of this study. Inhibition of P38 activation was sufficient to reduce hamster fibroblast cells death and apoptosis induced by moderate tunicamycin .…”

“…It is well known that the MAPK cascade is an important pathway in eukaryotic signal transduction networks, and it plays a key role in regulating many cytoplasmic functions and gene expression pathways. It was previously reported that UVA irradiation induces the phosphorylation of ERK, p38, and JNK . Our results showed that the p‐JNK/JNK ratio was unchanged after UVA irradiation.…”

“…ERK is a signal transduction protein that transmits mitogenic signals. It has been found that the phosphorylation levels of ERK in HDFs do not change if the cells are incubated for 12 hours after 5 J/cm 2 UVA irradiation, although the levels of p‐ERK were increased when HDFs were incubated for 24 hours after 20 J/cm 2 UVA irradiation . We observed that ERK phosphorylation was decreased after 12 J/cm 2 UVA treatment and incubation for 12 hours.…”

Combination of Natural Extracts and Photobiomodulation in Keratinocytes Subjected to UVA Radiation

“…In order to verify the protective effects of cycloheterophylin on fibroblasts after exposures to UVA, Huang et al . used a higher radiant exposure, 20 J cm −2 , but they started with approximately 70% cell damage. Similarly, Chan et al .…”

“…Huynh et al (19) found a 50% decrease in the viability of keratinocytes (HaCaT) with a radiant exposure of 20 J cm À2 results that corroborated those found in this study. In order to verify the protective effects of cycloheterophylin on fibroblasts after exposures to UVA, Huang et al (20) used a higher radiant exposure, 20 J cm À2 , but they started with approximately 70% cell damage. Similarly, Chan et al (10) used a radiant exposure of 20 J cm À2 in retinal epithelial cells, causing 50% cell death.…”