OBJECTIVE: The purpose of this study was to examine the protection afforded by 635-nm irradiation against ultraviolet (UV)-C-induced apoptosis in primary human gingival fibroblasts (hGFs). BACKGROUND DATA: UV irradiation is known to cause photoaging and cellular apoptosis of skin cells and is considered to be one of the leading causes of skin carcinogenesis. MATERIALS AND METHODS: To induce apoptosis, UV-C (100 mJ/cm2) was used to irradiate hGFs. To protect them from apoptosis, pretreatment with 635-nm irradiation was performed for 1 h immediately after cell plating 36 or 48 h before UV-C irradiation. The light source used for irradiation was a continuous-wave 635-nm LED laser emitting at 1 mW/cm2. Experimental samples were selected 24 h after UV-C irradiation. To measure the numbers of apoptotic cells, MTT assay and flow cytometric analyses were performed. For histomorphologic findings, Diff-Quick staining was carried out. Also, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were measured. RESULTS: In the present study, the number of apoptotic cells declined in the cells that were pretreated with 635-nm light irradiation in a time-dependent manner. In addition, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were significantly recovered by pretreatment with 635-nm irradiation. CONCLUSION: These results suggest that 635-nm visible light irradiation may be used as a protective tool to prevent UV-C-induced apoptosis.
OBJECTIVE: The purpose of this study was to examine the protection afforded by 635-nm irradiation against ultraviolet (UV)-C-induced apoptosis in primary human gingival fibroblasts (hGFs). BACKGROUND DATA: UV irradiation is known to cause photoaging and cellular apoptosis of skin cells and is considered to be one of the leading causes of skin carcinogenesis. MATERIALS AND METHODS: To induce apoptosis, UV-C (100 mJ/cm2) was used to irradiate hGFs. To protect them from apoptosis, pretreatment with 635-nm irradiation was performed for 1 h immediately after cell plating 36 or 48 h before UV-C irradiation. The light source used for irradiation was a continuous-wave 635-nm LED laser emitting at 1 mW/cm2. Experimental samples were selected 24 h after UV-C irradiation. To measure the numbers of apoptotic cells, MTT assay and flow cytometric analyses were performed. For histomorphologic findings, Diff-Quick staining was carried out. Also, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were measured. RESULTS: In the present study, the number of apoptotic cells declined in the cells that were pretreated with 635-nm light irradiation in a time-dependent manner. In addition, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were significantly recovered by pretreatment with 635-nm irradiation. CONCLUSION: These results suggest that 635-nm visible light irradiation may be used as a protective tool to prevent UV-C-induced apoptosis.