文章摘要
贺艳丽,王运萍,綦春蕾,赵淑华,李玲霞,周福兴,张 潍.ω-3脂肪酸对人滋养层细胞侵袭和血管生成的影响[J].,2023,(6):1010-1016
ω-3脂肪酸对人滋养层细胞侵袭和血管生成的影响
Effects of Omega-3 Fatty Acids on the Invasion and Angiogenesis of Human Trophoblast Cells
投稿时间:2022-08-18  修订日期:2022-09-15
DOI:10.13241/j.cnki.pmb.2023.06.003
中文关键词: ω-3脂肪酸  滋养层细胞  侵袭  血管生成  三结构域蛋白22  信号转导和转录激活因子1
英文关键词: ω-3 fatty acids  Trophoblast cells  Invasion  Angiogenesis  Tripartite motif-containing 22  Signal transducer and activator of transcription 1
基金项目:国家自然科学基金青年基金项目(82002735)
作者单位E-mail
贺艳丽 第四军医大学西京医院妇产科 陕西 西安 710032 lsing20Qin@126.com 
王运萍 第四军医大学西京医院妇产科 陕西 西安 710032  
綦春蕾 第四军医大学西京医院妇产科 陕西 西安 710032  
赵淑华 第四军医大学西京医院妇产科 陕西 西安 710032  
李玲霞 第四军医大学西京医院妇产科 陕西 西安 710032  
周福兴 第四军医大学西京医院妇产科 陕西 西安 710032  
张 潍 第四军医大学西京医院妇产科 陕西 西安 710032  
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中文摘要:
      摘要 目的:探讨ω-3脂肪酸对人滋养层细胞(HTR-8/SVneo)侵袭和血管生成的影响。方法:本实验设置了不同浓度二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)处理组,依次为0、1、50和100 μmol/L EPA组;0、1、50和100 μmol/L DHA组。各组HTR-8/SVneo细胞分别用相应浓度的EPA和DHA培养48 h。然后通过CCK-8法检测细胞增殖,Matrigel Transwell实验检测细胞侵袭。使用EPA和DHA处理的HTR-8/SVneo细胞的上清液培养人脐静脉内皮细胞(HUVEC)6 h,然后检测HUVEC的小管形成能力。通过qRT-PCR和Western blot检测HTR-8/SVneo细胞中三结构域蛋白22(TRIM22)、信号转导和转录激活因子1(STAT1)、p-STAT1(Tyr701)、基质金属蛋白酶2(MMP2)、MMP9和VEGF的表达。结果:与0 μmol/L EPA组或0 μmol/L DHA组相比,50 μmol/L EPA组、100 μmol/L EPA组、50 μmol/L DHA组和100 μmol/L DHA组的OD450nm 、侵袭细胞数量、MMP2和MMP9的蛋白相对表达量均升高(P<0.05)。与0 μmol/L EPA组或0 μmol/L DHA组相比,50 μmol/L EPA组、100 μmol/L EPA组、50 μmol/L DHA组和100 μmol/L DHA组的相对小管长度和VEGF蛋白相对表达量均升高(P<0.05)。与0 μmol/L EPA组或0 μmol/L DHA组相比,50 μmol/L EPA组、100 μmol/L EPA组、50 μmol/L DHA组和100 μmol/L DHA组的TRIM22 mRNA和蛋白相对表达量均升高,而STAT1 mRNA相对表达量和p-STAT1 (Tyr701)蛋白相对表达量均降低(P<0.05)。结论:ω-3脂肪酸处理可促进滋养层细胞的侵袭性和血管生成,其机制可能与TRIM22的上调和STAT1活性的抑制有关。
英文摘要:
      ABSTRACT Objective: To investigate the effects of omega-3 fatty acids on the invasion and angiogenesis of human trophoblast cells (HTR-8/SVneo). Methods: Different concentrations of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) groups were set up: 0 μmol/L EPA group, 1 μmol/L EPA group, 50 μmol/L EPA group and 100 μmol/L EPA group; 0 μmol/L DHA group, 1 μmol/L DHA group, 50 μmol/L DHA group and 100 μmol/L DHA group. The HTR-8/SVneo cells in each group were cultured with corresponding concentrations of EPA and DHA for 48 h. Then the cell proliferation was detected by the CCK-8 method, and the cell invasion was detected by the Matrigel Transwell test. Human umbilical vein endothelial cells (HUVEC) were cultured for 6 h with the supernatant of HTR-8/SVneo cells treated with EPA and DHA, and then the tubule forming ability of HUVEC was detected. The expression level of tripartite motif-containing 22 (TRIM22), signal transducer and activator of transcription 1 (STAT1), p-STAT1 (Tyr701), matrix metalloproteinase 2 (MMP2), MMP9, MMP9 and VEGF in HTR-8/SVneo cells were detected by qRT-PCR and Western blot. Results: Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, OD450 nm , number of invaded cells, and relative protein expression level of MMP2 and MMP9 in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and 100 μmol/L DHA group were increased (P<0.05). Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, the relative tubule length and the relative expression of VEGF protein in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and 100 μmol/L DHA group were increased (P<0.05). Compared with the 0 μmol/L EPA group or 0 μmol/L DHA group, the relative expression levels of TRIM22 mRNA and protein in the 50 μmol/L EPA group, 100 μmol/L EPA group, 50 μmol/L DHA group and 100 μmol/L DHA group were increased, while the relative expression of STAT1 mRNA and p-STAT1 (Tyr701) protein were decreased (P<0.05). Conclusion: Omega-3 fatty acid treatment can promote the invasiveness and angiogenesis of trophoblast cells. The mechanism may be related to the up-regulation of TRIM22 and the inhibition of STAT1 activity.
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