Human skin is influenced by ultraviolet-B (UV-B) irradiation. UV-B induces DNA damage and mitochondrial damage in epidermal keratinocytes； then accumulation of excessive DNA damage and damaged mitochondria finally leads to apoptosis. Recently, we investigated effective means to repair or to eliminate fatal damage leading to excessive apoptosis in UV-B-exposed normal human epidermal keratinocytes (NHEKs) . Concerning repair of DNA damage, we previously established a method for measuring activity of cellular DNA polymerase (pol) which synthesizes DNA strands in the repair system in NHEKs, and found that Rhodomyrtus tomentosa fruit extract, which has properties to protect epidermal keratinocytes from UV-B-induced apoptosis, enhanced activity of pol in UV-B-irradiated NHEKs. With regard to repair and elimination of mitochondrial damage, we focused on mitophagy, which is the cellular function to remove dysfunctional mitochondria by autophagy. In the present study, we detected mitophagy and evaluated mitochondrial reductase activity providing an indication of cell viability in UV-B-irradiated NHEKs. As a result of evaluating the influence of UV-B irradiation on mitophagy in NHEKs, we observed that mitophagy became weak after irradiation with 40 mJ/cm² UV-B. In addition, mitochondrial reductase activity also decreased at 24 h after irradiation. Following these results, we also found that Rhodomyrtus tomentosa fruit extract suppressed the UV-B-induced decrease in mitophagy and in mitochondrial reductase activity. Furthermore, we investigated influence of UV-B irradiation and effect of the extract on mitochondrial membrane potential in NHEKs to elucidate the mechanisms of modulating mitophagy. The results showed that the extract retained normal function of mitophagy by decreasing mitochondrial membrane potential in advance. In conclusion, it was suggested that the enhancement of inherent cellular DNA repair properties and the efficient elimination of the mitochondrial damage are essential for protecting the epidermal keratinocytes from UV-B-induced excessive apoptosis.