和厚朴酚抑制白血病U937细胞侵袭及血管新生作用

Honokiol inhibits the invasion and angiogenesis of U937 leukemia cells

目的探讨和厚朴酚(HNK)对人白血病U937细胞侵袭及血管新生作用的影响及其可能的分子机制。方法应用不同浓度的HNK处理U937细胞不同时间,用MTT法检测HNK对细胞增殖抑制作用;基质黏附试验检测HNK对U937细胞黏附功能的影响;TranswellTM小室检测HNK对U937细胞侵袭抑制作用。实时定量PCR(qRT-PCR)检测血管内皮生长因子(VEGF)、血管内皮生长因子受体1(VEGFR1)、基质金属蛋白酶9(MMP-9)mRNA水平变化。ELISA检测HNK处理U937细胞后上清VEGF蛋白表达水平。结果 HNK对U937的体外增殖有显著抑制作用,呈剂量和时间依赖性。低浓度HNK能够抑制U937细胞的黏附及侵袭能力。不同浓度HNK处理U937细胞24 h后,细胞VEGF、VEGFR1及MMP-9表达水平呈剂量依赖性下调。结论 HNK可能通过抑制VEGF、VEGFR1及MMP-9表达,抑制U937细胞侵袭及血管新生功能。

Objective To investigate the inhibiting effect of Honokiol （HNK） on the invasion and angiogenesis in U937 leukemia cells and the molecular mechanism. Methods After treated with different concentrations of HNK, the growth inhibition rate of U937 cells was determined by M＇l-r assay, and for the adhesion and invasion abilities were assessed using cell matrix adhesion technique and TranswellTM assay, respectively. VEGF, VEGFR1 and MMP-9 mRNA expression levels were detected by real-time quantitative RT-PCR （qRT-PCR）. VEGF protein levels were determined by ELISA. Results HNK could significantly inhibit the proliferation of U937 cells in a time- and dose-dependent manner. The adhesion and invasion abilities of U937 cells were suppressed after treated with a low concentration of HNK. The expressions of VEGF, VEGFR1 and MMP-9 were down-regulated by HNK in a dose-dependent manner. Conclusion HNK can inhibit the invasion and angiogenesis of U937 cells via down-regulating VEGF, VEGFR1 and MMP-9 expressions.