PURPOSE: We investigated the effects of short-term exposure to triamcinolone on cultured choroidal fibroblast (CFB) cells and retinal pigment epithelial (RPE) cells. METHODS: To evaluate the effect of triamcinolone on cell proliferation, CFB and RPE cells were divided into three groups: a short-term exposure group; a longterm exposure group, and a non-treated control group. Cells in the short-term exposure group were briefly exposed (5, 15 or 30 mins) to triamcinolone (0.01 mg/ml, 1 mg/ml or mitomycin C (0.01 microg/ml, 1 microg/ml). Cells in the longterm exposure group were continuously incubated in culture medium containing the drug until assessment. The control group was cultured without drugs. Cell viability and the number of cells were assessed at day 5 after exposure. To investigate the direct toxicity of triamcinolone on confluent RPE cells, completely confluent cells were exposed to the drugs in the manner as described above. Cell viability was determined on days 0, 3 and 5 after treatment. RESULTS: In the short-term exposure group, 1 mg/ml triamcinolone caused a significant reduction in the proliferation of CFB and RPE cells. The proliferation of CFBs decreased even with exposure to 0.01 mg/ml triamcinolone. In the longterm exposure group, triamcinolone and mitomycin C reduced the proliferation of both CFB and RPE cells. Even very short periods of exposure to triamcinolone caused a significant reduction in the viability of completely confluent RPE cells. CONCLUSIONS: Even short periods of exposure to triamcinolone inhibited the proliferation of fibroblasts and RPE cells and were significantly toxic to completely confluent RPE cells.
PURPOSE: We investigated the effects of short-term exposure to triamcinolone on cultured choroidal fibroblast (CFB) cells and retinal pigment epithelial (RPE) cells. METHODS: To evaluate the effect of triamcinolone on cell proliferation, CFB and RPE cells were divided into three groups: a short-term exposure group; a longterm exposure group, and a non-treated control group. Cells in the short-term exposure group were briefly exposed (5, 15 or 30 mins) to triamcinolone (0.01 mg/ml, 1 mg/ml or mitomycin C (0.01 microg/ml, 1 microg/ml). Cells in the longterm exposure group were continuously incubated in culture medium containing the drug until assessment. The control group was cultured without drugs. Cell viability and the number of cells were assessed at day 5 after exposure. To investigate the direct toxicity of triamcinolone on confluent RPE cells, completely confluent cells were exposed to the drugs in the manner as described above. Cell viability was determined on days 0, 3 and 5 after treatment. RESULTS: In the short-term exposure group, 1 mg/ml triamcinolone caused a significant reduction in the proliferation of CFB and RPE cells. The proliferation of CFBs decreased even with exposure to 0.01 mg/ml triamcinolone. In the longterm exposure group, triamcinolone and mitomycin C reduced the proliferation of both CFB and RPE cells. Even very short periods of exposure to triamcinolone caused a significant reduction in the viability of completely confluent RPE cells. CONCLUSIONS: Even short periods of exposure to triamcinolone inhibited the proliferation of fibroblasts and RPE cells and were significantly toxic to completely confluent RPE cells.