Effects of red LED on UVA induced photodamage in Human fibroblasts

• Main Authors: Pei-Yun Ho, 何珮芸
• Other Authors: Hsin-Su Yu
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/57997094500305627991

碩士 === 高雄醫學大學 === 生理及分子醫學研究所 === 99 === Ultraviolet A (UVA) contains wavelength of 320~400nm that can pass through the epidermis to the dermis, the location of fibroblasts. Fibroblast is the major extracellular matrix producer that secretes collagen to function as the major supporter in skin tissue. Studies have shown that reactive oxygen species (ROS) produced by fibroblasts are increased under UVA irradiation and lead to up-regulation of MMP-1 protein via MAPK pathway, which results in collagen degradation and photo damage. However, light with specific wavelength can also help skin tissue to be recovered from photo damage in skin. Traditional phototherapy uses lasers or pulsed dye laser (PDL) to reverse or repair sun-induced damages, which is effective but painful. Recently, Light-emitting diode (LED) is discovered as a new way for light therapy. Phototherapeutic LED-based systems have been shown to be an effective, safe, well-tolerated and painless treatment. Clinical studies have shown that low-energy visible light (LEVL), such as yellow LED (595nm) and red LED (630nm) have beneficial effects on aging prevention.Several studies also reported that cellular functions could be influenced by visible light (400–700 nm) irradiation. However, the exact beneficial effects of LED irradiation still remain elusive. To better understand how red LED prevent UVA-induced cell damage, we investigated the effects of LED irradiation on UVA-induced cell damage. In this study, we used fibroblasts which were isolated from humen’ foreskins and the primary fibroblasts were sub-cultured for the subsequent experiments. We used MTS to observe cell viability. ROS (H2O2) production was measured by flow cytometry. The protein levels of p-JNK, p-P38, and MMP-1 were each quantified by Western blot. Our data showed that under UVA irradiation, mitochondria activity was declined accompanied with an increase of ROS in fibroblasts, and MMP-1 mRNA and protein expression level is up-regulated. Cells pretreated with LED and irradiated with UVA had higher cell viability compared to non-LED pretreatment group. We also demonstrated that intracellular ROS production and MMP-1 protein level were altered by UVA irradiations which were reversed by LED pretreatment. Furthermore, we observed that LED pre-treatment groups showed significant decrease in p-JNK level while it was not observed in p-P38 level under the UVA irradiation. We also exploited ROS and JNK inhibitors to show that LED protection against UVA-induced injury was mediated through ROS-induced JNK pathway. These results suggested that LED irradiation protected human dermal fibroblasts cells from UVA damage through regulation of the MAP kinase pathway.