Objective To investigate the effect and mechanism of arsenic trioxide on pulmonary fibrosis (PF).Methods Fibroblast cells NIH3T3 in logarithmic phase were randomly divided into control group and observed group 1, observed group 2, then were cultured in DMEM medium supplemented with 0,2, 4 μmol / L of As2O3 for 24 hs and 48 hs respectively.The inhibition rate(IR) of cell proliferation was detected by MTT assay and the cell cycle was detected by flow cytometry, the ultrastructure of the cells and morphological changes of nucleus were observed using transmission electronmicroscopy and Hoechst staining.Results Cell proliferation IR in observed groupl and group 2 was significantly higher than that in control group,and especially higher in observed group 2 and the ones treated for 48 hs( all P ＜ 0.01 ); Compared with control group, G0/G1 phase ratios increased and G2/ M phase ratios decreased significantly in observed group 1 and observed group 2, especially in observed group 2 ( all P ＜0.01 ) ;Cells treated by As2O3 presented some morphological features of the early and mid-term apoptosis changes ( intact cell structure, chromatin margination and chromatin condensation).Conclusion As2O3 can inhibit proliferation and promote apoptosis of fibroblast cell line NIH3T3 , which provides new ideas for the treatment of PF.%目的 探讨三氧化二砷(As2O3)的抗肺纤维化(PF)作用及其机制.方法 将对数生长期成纤维细胞株NIH3T3随机分为对照组及观察1组、观察2组,分别用含0、2、4 μmol/L As2O3的DMEM培养液处理24 h和48 h,采用四甲基偶氮唑蓝(MTT)法检测细胞增殖抑制率(IR),流式细胞术检测细胞周期分布,透射电镜和Hoechst染色方法观察细胞超微结构及细胞核形态变化.结果 观察1组和观察2组细胞增殖IR均显著高于对照组,尤以作用48 h时和观察2组为著(P均＜0.01);观察1组和观察2组G0/G1期细胞显著多于对照组,而G2/M期细胞显著少于对照组,尤以观察2组为著(P均＜0.01);观察1组和观察2组细胞具有早、中期凋亡形态学特征(细胞膜结构完整、细胞质浓缩、染色质边集、固缩).结论 As2O3可抑制肺成纤维细胞株NIH3T3增殖并促进其凋亡,此为临床PF治疗提供了新思路.
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