Protective effect of pre- and post-vitamin C treatments on UVB-irradiation-induced skin damage

Masayuki Yoshida,Akihito Ishigami,Hajime Ohsawa,Kisaburo Nagata,Norikatsu Saito,Tomoko Funakoshi,Yasunori Sato,Saki Kawashima,Katsumi Kurita

doi:10.1038/s41598-018-34530-4

Abstract

Several studies have reported the effects of vitamin C (L-ascorbic acid, AA) on ultraviolet B (UVB)-induced cell damage using cultured keratinocytes. However, the epidermis consists of multiple cell layers, and the effect of AA on UVB-induced damage to the human epidermis remains unclear. Therefore, we investigated the effect of AA on UVB-induced skin damage using reconstituted human epidermis. The reconstituted human epidermal surface was treated with 100 and 500 mM AA and cultured for 3 h before (pre-AA treatment) or after (post-AA treatment) 120 mJ/cm2 UVB irradiation. Pre- and post-AA treatments of the epidermal surface suppressed UVB-induced cell death, apoptosis, DNA damage, reactive oxygen species (ROS) production, and the inflammatory response by downregulating tumour necrosis factor-α (TNF-α) expression and release. Moreover, the pre-AA treatment was more effective at preventing UVB-induced skin damage than the post-AA treatment. In summary, pre- and post-AA treatments of the epidermis prevent UVB-induced damage.

Highlights

Solar ultraviolet (UV) radiation is the most important environmental factor causing cancer and photoaging, such as wrinkle formation, acute erythema, and tanning of human skin[1,2,3]
In this study, we investigated the effect of AA on ultraviolet B (UVB)-induced skin damage using the reconstituted human epidermis
AA was detected in the medium under the membrane when 10, 100, 500, and 1000 mM AA were applied for 3 and 6 h, but it was not detected in media from samples that were not treated with AA (Fig. 1c)

Summary

Introduction

Solar ultraviolet (UV) radiation is the most important environmental factor causing cancer and photoaging, such as wrinkle formation, acute erythema, and tanning of human skin[1,2,3]. AA reduces UVB-induced ROS production and prevents ROS-mediated cell death and oncogenesis in epidermal keratinocytes[18,19]. Several studies have reported the effects of AA on UVB-induced cell damage using cultured keratinocytes, the epidermis consists of multiple cell layers. SMP30 is an essential enzyme in the AA biosynthetic pathway[17] Using this SMP30 knockout hairless mouse model, we previously reported that AA deficiency led to epidermal atrophy and the development of excessive skin pigmentation in AA-insufficient SMP30 knockout hairless mice following exposure to UVB irradiation[21]. The effect of AA on UVB-induced damage to the human epidermis remains unclear. In this study, we investigated the effect of AA on UVB-induced skin damage using the reconstituted human epidermis

Methods

Results

Conclusion