论文部分内容阅读
[目的]探讨三氧化二砷(ATO)对增生性瘢痕成纤维细胞(HSF)增殖及细胞外基质代谢的影响.[方法]0 μmol/L(对照组)、2 μmol/L、4 μmol/L、8 μmol/L的ATO作用HSF 24、48、72 h后,MTT法检测细胞活力,流式细胞术检测细胞凋亡及细胞周期,酶联免疫吸附(ELISA)法检测Ⅰ型胶原蛋白(CoLⅠ)和CoL Ⅲ含量,western blot检测基质金属蛋白酶-1(MMP-1)、MMP-13及基质金属蛋白酶组织抑制剂-1(TIMP-1)表达.[结果]与对照组比较,2、4、8 μmol/L的 ATO显著降低HSF细胞活力(P<0.01),提高细胞早期凋亡率及晚期凋亡率,使细胞周期阻滞在G1期(P<0.01),降低细胞中CoLⅠ、CoL Ⅲ含量(P<0.01),下调TIMP-1表达,上调MMP-1,MMP-13表达(P<0.01);与2 μmol/L 比较,4、8 μmol/L的ATO能显著显著降低HSF细胞活力(P<0.01),提高细胞早期凋亡率及晚期凋亡率,使细胞周期阻滞在G1期(P<0.01),降低细胞中CoLⅠ、CoL Ⅲ含量(P<0.01),下调TIMP-1表达(P<0.01),上调MMP1及MMP13表达(P<0.01);与4 μmol/L 比较, 8 μmol/L的ATO能显著降低HSF细胞活力(P<0.01),提高细胞早期凋亡率及晚期凋亡率,使细胞周期阻滞在G1期(P<0.01),降低细胞中CoLⅠ、CoLⅢ含量(P<0.01),下调TIMP-1表达(P<0.01),上调MMP1及MMP13表达(P<0.01).[结论]ATO能显著的抑制HSF增殖及细胞外基质合成,促进细胞外基质降解.“,”[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.