论文部分内容阅读
目的:观察金荞麦抗肿瘤提取物(FR)、苦参抗肿瘤提取物(MA)对肺癌PG细胞-血管内皮(HU-VEC)黏附作用的影响,并探讨其抗肿瘤转移机制。方法:运用MTT检测FR/MA单药及联合用药对高转移肺癌PG细胞增殖的作用,以荧光标记PG-HUVEC黏附模型考察FR/MA单药及联合用药抗肿瘤细胞的黏附能力,用Western blotting、流式细胞仪检测FR/MA单药及联合用药对黏附分子表达的影响。结果:FR/MA单药及联合用药均剂量依赖性抑制PG细胞增殖(P<0.05);在一定浓度范围内,FR/MA单药及联合用药显著抑制PG-HU-VEC相互黏附能力并有剂量依赖性(P<0.01);FR/MA联合用药显著抑制黏附分子CD44、CD49、ICAM-1及E-selectin的表达(P<0.01)。结论:FR/MA具有抗PG-HUVEC相互黏附作用;降低细胞表面黏附分子的表达,抑制肿瘤细胞在血管壁着床可能是其抗肿瘤转移的作用机制之一。
OBJECTIVE: To observe the effects of anti-tumor extract of golden buckwheat (FR) and anti-tumor extract (MA) of Sophora flavescens on the adhesion of lung cancer PG cell-vascular endothelial (HU-VEC), and to explore its anti-tumor metastasis mechanism. METHODS: MTT was used to detect the effect of FR/MA single agent and combination therapy on the proliferation of high metastatic lung cancer PG cells. Fluorescence-labeled PG-HUVEC adhesion model was used to investigate the anti-tumor cell adhesion ability of FR/MA single drug and combination therapy. Western blotting was used. Flow cytometry was used to examine the effect of FR/MA monotherapy and combination therapy on the expression of adhesion molecules. RESULTS: FR/MA monotherapy and combination therapy inhibited the proliferation of PG cells in a dose-dependent manner (P<0.05). Within a certain concentration range, FR/MA monotherapy and combination therapy significantly inhibited the mutual adhesion ability of PG-HU-VEC. In a dose-dependent manner (P<0.01), FR/MA combination therapy significantly inhibited the expression of adhesion molecules CD44, CD49, ICAM-1, and E-selectin (P<0.01). Conclusion: FR/MA has anti-PG-HUVEC mutual adhesion; decreasing the expression of cell surface adhesion molecules and inhibiting tumor cells in the vascular wall implantation may be one of the mechanisms of its anti-tumor metastasis.