| Summary: | 碩士 === 國防醫學院 === 海底醫學研究所 === 93 === The diabetes causes the patient with slow wound healing even facing the fate of amputation due to the peripheral neuropathy, peripheral vascular diseases and immunopathy. At the same time the foot ulceration is also one of the main reasons to cause the diabetes death. Fibroblast plays a key role in the course of healing the wound. Researches showed that fibroblast sampled from diabetic foot ulceration revealed slower growth rate than the normal cells. In addition, high glucose also suppressed proliferation of fibroblast and collagen synthesis. The detailed mechanism is largely unknown, but has been proposed to be the increase of free radicals due to high glucose exposure. Hyperbaric oxygen therapy (HBOT) has been widely used in treating the diabetic wounds. It has been shown that HBOT could enhance proliferation of fibroblast, increase synthesis of collagen, and accelerate healing of chronic wound. Therefore, in this study we adapted a model of cell culture to investigate the effect of high glucose and hyperoxia on the human skin fibroblast. Cells (Detroit 551) were cultured in high glucose medium (D-glucose 25 mM and 50mM) for either 3 or 7 days to evaluate cell survival rate, cell proliferation, and cell death. The result showed that high glucose reduced the survival rate of fibroblast, inhibited cell proliferation, and increased cell apoptosis and necrosis. In other groups, while fibroblasts was cultured in high glucose, hyperoxia (95% oxygen or 2.5 ATA HBOT) was delivered 90 min each day for 3 or 7 days. The result showed that hyperoxia reduced cell survival rate, suppressed cell proliferation, and caused cell death of human skin fibroblast. Both high glucose and hyperoxia caused significant increase of superoxide production. In conclusion, high glucose and hyperoxia cause significant damage to the human skin fibroblast synergically. This toxic effect may be due to production of free radicals.
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