|
|
Effect of Arsenic Trioxide on Proliferation and Extracellular Matrix Metabolism of Hypertrophic Scar Fibroblasts |
ZHANG Qin-xue |
Department of burns and plastic surgery, the First Affiliated Hospital of PLA General Hospital, Beijing 110048 |
|
|
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.
|
Received: 06 March 2017
|
|
|
|
|
[1] Zhu Z, Ding J, Tredget EE. The molecular basis of hypertrophic scars[J].Burns Trauma,2016,4:2. [2] 柯俐安, 杨军. 增生性瘢痕无创性评估策略及方法[J].组织工程与重建外科杂志, 2016,12(4):262-265. [3] 黄鹂, 刘江山. 不同治疗方案在面部痤疮凹陷性瘢痕患者中的疗效对比[J].医学临床研究, 2016,33(5):922-925. [4] 张雪, 兰东, 宁淑华, 等. A型肉毒毒素对增生性瘢痕成纤维细胞的抑制作用及机制[J].重庆医学, 2017,47(5):580-582. [5] 孙桂芳, 张晓芬, 陈亚峰, 等. 生肌玉红膏通过下调TGF-β1/Smads抑制人增生性瘢痕成纤维细胞增殖和胶原分泌[J].时珍国医国药, 2016,27(7):1590-1593. [6] 王静, 甄建中, 李艳萌, 等. 三氧化二砷在慢性粒细胞白血病治疗中的作用机制研究进展[J].山东医药, 2014,54(47):96-98. [7] 刘欢, 那仁满都拉. 三氧化二砷治疗癌症机制研究进展[J].中国现代应用药学, 2013,30(3):338-342. [8] 韩剑宇, 庞建华, 陈伟华, 等. 三氧化二砷对增生性瘢痕成纤维细胞增殖和胶原合成的影响[J].哈尔滨医科大学学报, 2014,48(3):182-185. [9] 张百红, 岳红云. 肿瘤检查点相关研究进展[J].癌症进展, 2015,13(3):260-264. [10] 付朝霞, 汝童, 王珊珊, 等. 三氧化二砷联合氨氯地平对肝癌HepG2细胞体外作用的实验研究[J].现代生物医学进展, 2015,15(4):614-617. [11] 谢庆环, 梁玉芬, 赵萍, 等. 三氧化二砷对膀胱癌细胞BIU-87细胞增殖、凋亡的作用[J].中国地方病防治杂志, 2016,31(9):1044-1045. [12] 王愿, 杨洁, 李杰, 等. 三氧化二砷对K562细胞增殖抑制作用及其机制研究[J].中国实验血液学杂志, 2017,25(1):90-93. [13] 边曦, 吴江群, 聂兴举, 等. 氧化苦参碱对人瘢痕成纤维细胞前胶原及纤维粘连蛋白表达的影响[J].中国中西医结合杂志, 2012,32(10):1390-1393. [14] 孔德平, 陈凯. 5-氟尿嘧啶对增生性瘢痕的作用研究[J].重庆医学, 2015,44(8):1029-1031. [15] Shi HX, Lin C, Lin BB,et al.The anti-scar effects of basic fibroblast growth factor on the wound repair in vitro and in vivo[J].PLoS One,2013,8(4):e59966. |
|
|
|