Abstract:

Objective To investigate the effects of pentoxifylline on the cell proliferation of, collagen synthesis and TGF-βl expression by human fibroblasts derived from keloid. Methods Skin samples were obtained from the lesions of 3 patients with keloid and normal skin of 3 human controls followed by primary culture of fibroblasts. Fibroblasts of 5th to 8th generation were cultured with pentoxifylline of 0.1 to 3 g/L for various durations. Then, MTT assay was performed to detect the cell proliferation of fibroblasts, double antibody sandwich-enzyme linked immunosorbent assay （ELISA） to measure the expression of TGF-βl, and reverse-transcription PCR to examine the mRNA expressions of procollagenⅠand Ⅲ in these fibroblasts. Results The pentoxifylline of 0.1 to 2 g/L markedly inhibited the proliferation of fibroblasts derived from keloid lesions and normal skin, in a dose- and time-dependent manner, with the strongest effect observed in fibroblasts treated with pentoxifylline of 2 g/L. A significant reduction was induced in the TGF-βl mRNA expression in keloid- and normal skin-derived fibroblasts by pentoxifylline of 0.5 to 2 g/L （all P < 0.01）, and in the mRNA expression of procollagenⅠand Ⅲ by pentoxifylline of 1 and 2 g/L （P < 0.05 or 0.01）. Concretely, the relative mRNA expression level of procollagenⅠand Ⅲ was 0.873 ± 0.077, 0.571 ± 0.050 respectively in keloid fibroblasts respectively, and 0.473 ± 0.035, 0.370 ± 0.045 in the control fibroblasts, after treated with pentoxifylline of 1 g/L, 0.750 ± 0.036 and 0.433 ± 0.045 respectively in keloid-derived fibroblasts, 0.390 ± 0.030 and 0.250 ± 0.123 respectively in the control fibroblasts, after treated with pentoxifylline of 2 g/L, significantly lower than that in the keloid-derived （1.216 ± 0.061 and 0.953 ± 0.060） and control （0.836 ± 0.080 and 0.776 ± 0.041） fibroblasts without treatment. Conclusion Pentoxifylline shows an evident suppressive effect on the cell proliferation of, as well as the expression of TGF-βl and procollagenⅠand Ⅲ in fibroblasts derived from keloid lesions and normal skin.

Key words: I, III procollagen mRNA.