厚朴酚葡萄糖苷对人乳腺癌细胞增殖、侵袭、迁移的影响

目的:探索联苯型新木脂素类化合物厚朴酚葡萄糖苷（magnolol-2-O-β-D-glucopyranoside，Mag-glu）对人乳腺癌细胞增殖、侵袭、迁移能力的影响，并对其可能机制进行研究。方法:MTT法检测化合物对MCF-7和MDA-MB-231细胞增殖的影响；细胞划痕实验和Transwell小室法检测化合物对人乳腺癌细胞运动、侵袭和迁移能力的影响；Western blotting法检测化合物对缺氧诱导因子1α（HIF-1α）、基质金属蛋白酶-9（MMP-9）和环氧化酶2（COX-2）蛋白表达的影响。结果:Mag-glu具有抑制MCF-7和MDA-MB-231细胞增殖的作用，且呈现浓度和时间依赖性。划痕实验结果表明，经过不同浓度的Mag-glu处理MDA-MB-231细胞24 h后，细胞水平运动运动能力明显下降（P<0.01）。Transwell结果显示，经过不同浓度的Mag-glu处理细胞24 h和48 h后，细胞迁移和侵袭能力显著下降。Western blotting结果显示，随着Mag-glu浓度的增加，HIF-1α、MMP-9、COX-2的表达均下调。结论:Mag-glu在体外能够抑制人乳腺癌细胞的增殖、侵袭和迁移，其机制可能是抑制了HIF-1α信号途径，导致其下游顾客蛋白COX-2和MMP-9的表达下调有关。

Effect of magnolol glucoside on the proliferation,invasion and migration of human breast cancer cells

Objective: To investigate the effects of magnolol-2-O-β-D-glucopyranoside(Mag-glu) on the proliferation,invasion and migration of human breast cancer cells,and its possible mechanism.Methods: The effects of Mag-glu on the proliferation of MCF-7 and MDA-MB-231 cells were detected using MTT assay.The effects of Mag-glu on the migration and invasion ability of human breast cancer cells were analyzed using the wound healing assay and transwell assay,respectively.The effects of Mag-glu on the expression levels of hypoxia-inducible factor 1α(HIF-1α),matrix metalloproteinase-9(MMP-9) and cyclooxygenase-2(COX-2) were detected using Western blotting.Results: Mag-glu could inhibit the proliferation of MCF-7 and MDA-MB-231 cells in a concentration-and time-dependent manner.The migration ability of MDA-MB-231 cells decreased significantly after 24 h of treatment with Mag-glu(P<0.01).Transwell assay results showed that cell migration and invasion abilities significantly decreased after 24 h and 48 h of treatment with different concentrations of Mag-glu.The expression levels of HIF-1α,MMP-9 and COX-2 down-regulated with the increasing of the concentration of Mag-glu.Conclusions: Mag-glu can inhibit the proliferation,invasion and migration of human breast cancer cells in vitro,the mechanism of which may be inhibiting the HIF-1α signaling pathway to lead to the down-regulated expression of COX-2 and MMP-9.