| 董松涛,王力,张红梅,等.海洋溴酚BTDE抑制内皮细胞血管生成的研究（英文）[J].中国海洋药物,2023,42(6):48-54. |
| 海洋溴酚BTDE抑制内皮细胞血管生成的研究（英文） |
| Marine bromophenol BTDE inhibits endothelial angiogenesis through affecting tumor cell and tumor associated macrophage |
| 投稿时间：2022-05-25 修订日期：2022-07-04 |
| DOI：10.13400/j.cnki.cjmd.2023.06.024 |
| 中文关键词: 溴酚 血管生成 条件培养基 |
| English Keywords:bromophenols anti-angiogenesis conditioned medium |
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| 中文摘要: |
| 目的 探究海洋溴酚化合物双（2,3,6-三溴-4,5-二羟基苄基）醚（BTDE）处理肿瘤细胞和肿瘤相关巨噬细胞所获得的条件培养基对内皮细胞血管生成的影响。方法 MTT法检测BTDE对肿瘤相关巨噬细胞RAW264.7增殖的影响；Transwell实验检测BTDE对细胞迁移和侵袭的影响；明胶酶谱法检测BTDE对细胞分泌的基质金属蛋白酶9（MMP9）活性的影响；Western Blot检测BTDE对细胞中β-catenin、VEGF表达的影响；体外获取BTDE处理肺癌A549后的条件培养基（BTDE/A549-CM）和处理肿瘤相关巨噬细胞RAW264.7后的条件培养基（BTDE/RAW264.7-CM），采用Transwell和Tube formation实验检测条件培养基对人脐静脉内皮细胞HUVEC迁移和成管的影响。结果 BTDE抑制RAW264.7细胞的迁移、侵袭和分泌的MMP9活性；BTDE/A549-CM和BTDE/RAW264.7-CM抑制HUVEC细胞的迁移和血管生成，血管内皮细胞的血管生成率在5 μM和10 μM BTDE/A549-CM处理下为75.0％和23.8％，在2.5 μM，5 μM和?10 μM BTDE/RAW264.7-CM处理下为54.1％，35.69％和18.8％。 结论 海洋溴酚BTDE处理肺癌细胞A549和肿瘤相关巨噬细胞RAW264.7后的条件培养基能够抑制血管内皮细胞HUVEC的迁移和血管生成，提示BTDE有潜力发展为临床抗肿瘤血管生成治疗药物。 |
| English Summary: |
| Objective To study the effect on endothelial angiogenesis of conditioned medium from bis (2,3,6-tribromo-4,5-dihydroxybenzyl) ether (BTDE)-treated tumor cell or tumor associated macrophage. Methods MTT assay was used to explore the cytotoxic of BTDE on tumor associated macrophage RAW264.7; Transwell assay was used to evaluate the migration and invasion abilities of RAW264.7; Gelatin zymography assay was used to detect matrix metalloproteinase 9 (MMP9) activity of RAW264.7; Western blot assay was used to estimate β-catenin and VEGF expression of RAW264.7; Conditioned medium from BTDE-treated lung cancer cell A549 (BTDE/A549-CM) or tumor associated macrophage RAW264.7 (BTDE/RAW264.7-CM) was obtained in vitro, and its effect on the migration, tube forming abilities of human umbilical vein endothelial cell (HUVEC) was explored by transwell and tube formation assay. Results BTDE suppressed the migration, invasion and MMP9 activity of RAW264.7, what’s more, BTDE/A549-CM and BTDE/RAW264.7-CM inhibited the migration and tube formation of HUVEC, and the length of tube-like structures dropped to 75.0％ and 23.8％ with 5 μM and ?10 μM BTDE/A549-CM treatment, and to 54.1％, 35.69％ and 18.8％ with 2.5 μM, 5 μM and 10 μM BTDE/RAW264.7-CM treatment. Conclusion Conditioned medium from BTDE-treated lung cancer cell A549 or tumor associated macrophage RAW264.7 inhibited endothelial cell angiogenesis, indicating that BTDE could be developed as a potential candidate for future antitumor angiogenesis therapy. |
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