Abstract：【Objective】To explore effect of arsenic trioxide (ATO) on proliferation and extracellular matrix metabolism of hypertrophic scar fibroblasts (HSF). 【Methods】HSF viability was measured by MTT assay after cell was cultured with 0, 2, 4, 8 μmol/L dose of ATO. Cell apoptosis and cell cycle was measured by flow cytometry. The level of CoLⅠ and CoL Ⅲ was detected by enzyme linked immunosorbent assay (ELISA). The expression of matrix metalloproteinase-1 (MMP-1) and MMP-13, and tissue inhibitors of matrix metalloproteinases-1 (TIMP-1) was detected by western blot. 【Results】Compared to the no-added- ATO control group, 2, 4, 8 μmol/L dose of ATO reduced cell viability (P＜0.01), increased cell early apoptotic rate and late apoptotic rate (P＜0.01), made cell cycle arrested in the G1 phase (P＜0.01), reduced the level of CoLⅠ and CoL Ⅲ (P＜0.01), down-regulated the expression of TIMP-1 (P＜0.01) and up-regualted the expression of MMP-1, MMP-13 (P＜0.01). Compared to 2 μmol/L, 4and 8 μmol/L doses of ATO reduced cell viability (P＜0.01), increased cell early apoptotic rate and late apoptotic rate (P＜0.01), made cell cycle arrested in the G1 phase (P＜0.01), reduced the level of CoLⅠ and CoL Ⅲ (P＜0.01), down-regulated the expression of TIMP-1 (P＜0.01) and up-regualted the expression of MMP-1, MMP-13 (P＜0.01). Compared to 4 μmol/L, 8 μmol/L dose of ATO reduced cell viability (P＜0.01), increased cell early apoptotic rate and late apoptotic rate (P＜0.01), made cell cycle arrested in the G1 phase (P＜0.01), reduced the level of CoLⅠ and CoL Ⅲ (P＜0.01), down-regulated the expression of TIMP-1 (P＜0.01) and up-regualted the expression of MMP-1, MMP-13 (P＜0.01). 【Conclusion】The results showed that ATO significantly inhibited the proliferation of HSF, reduced the synthesis of extracellular matrix, and promoted the degradation of extracellular matrix.
2017, Vol. 34 
