沙利度胺对子宫内膜异位症患者内膜间质细胞的影响及其机制  

Effects of thalidomide on endometrial stromal cells in patients with endometriosis and its mechanism

作　　者：李宁[1] 彭兴[2] 黎丹戎[3] 尧良清[4] 黄玉葵[1] 范余娟[5] 

机构地区：[1]广西南宁市妇幼保健院妇科,南宁市530001 [2]广西医科大学药学院,南宁市530021 [3]广西医科大学附属肿瘤医院肿瘤实验研究中心,南宁市530021 [4]复旦大学附属妇产科医院妇科,上海市200011 [5]广西医科大学第一附属医院妇科,南宁市530021

出　　处：《广西医学》2016年第8期1062-1067,1100,共7页Guangxi Medical Journal

基　　金：广西科学研究与技术开发计划(桂科攻12300016);广西南宁市科技局项目(20133174)

摘　　要：目的探讨沙利度胺对子宫内膜异位症(EMT)患者内膜间质细胞(ESC)的增殖、迁移运动、修复及体外侵袭能力的影响及其作用机制。方法体外原代培养EMT患者的ESC,加入不同浓度沙利度胺(500.00、250.00、125.00、62.50、31.25μg/ml)分别作用24 h、48 h后,应用噻唑蓝法测定ESC的抑制率。另取ESC分为空白组(沙利度胺0μg/ml)、15μg/ml沙利度胺组、30μg/ml沙利度胺组,分别应用划痕实验、Transwell小室实验测定沙利度胺对ESC迁移运动及修复能力、体外侵袭能力的影响,流式细胞仪检测在沙利度胺作用24 h后ESC的凋亡率,酶联免疫吸附试验实验检测沙利度胺对ESC血管内皮生长因子(VEGF)蛋白表达的影响。结果 15、30μg/ml沙利度胺组细胞的迁移及修复能力、穿膜细胞数较空白组下降,细胞凋亡率较空白组升高(P<0.05);细胞抑制率随沙利度胺作用的浓度升高而升高(P<0.05);15、30μg/ml沙利度胺组细胞VEGF蛋白表达量明显低于空白对照组(P<0.05)。结论沙利度胺可抑制人EMT患者ESC的增殖、迁移运动和体外侵袭能力,并可以诱导细胞凋亡,其机制可能是下调细胞VEGF蛋白分泌。Objective To explore the effects of thalidomide on the proliferation, migration motion, repair and invasive ability in vitro of endometrial stromal cells（ESCs） in patients with endometriosis（EMT） and its mechanism. Methods The ESCs of patients with EMT primarily cultured in vitro,and were treated with various concentrations （500.00,250.00,125.00,62.50 and 31.25 μg/ml） of thalidomide for 24 and 48 hours respectively. Methyl thiazolyl tetrazolium method was used to detect the inhibition rate of ESCs. Another ESCs were divided into blank group（0 μg/ml thalidomide） , 15μg/ml thalidomide group and 30 μg/ml thalidomide group. Scratch-wound assay and Transwell assay were used to determine the effects of thalidomide on the abilities of migration motion and repair, and invasive ability in vitro of ESCs respectively. The apoptosis rates of ESCs were analyzed by flow cytometry after 24 hours of intervention with thalidomide. The effect of thalidomide on the expression of vascular endothelial growth factor （VEGF） protein of ESCs was detected by enzyme-linked immunosorbent assay. Results Compared to the blank group, the abilities of migration and repair, transmembrane cells decreased and cell apoptosis rate increased in the 15 and 30μg/ml thalidomide groups（ P 〈 0.05 ）. The cell inhibition rate was elevated with the increase of the intervention concentration of thalidomide（ P 〈0.05 ）. The expression of VEGF protein in the 15 or 30 μg/ml thalidomide groups was significantly lower than that in the blank control group （ P 〈 0.05 ）. Conclusion Thalidomide can inhibit the abilities of proliferation and migration motion, and invasive ability in vitro of ESCs in patients with EMT, and can induce the cell apoptosis. And the mechanism may be related to down-regulation of the secretion of VEGF protein in cells.

关 键 词：子宫内膜异位症 沙利度胺 内膜间质细胞 血管内皮生长因子 细胞增殖 迁移 侵袭 

分 类 号：R711.71[医药卫生—妇产科学]