诺帝对人恶性胶质瘤细胞U87甲酰化肽受体功能的影响

探讨手性化合物诺帝对人恶性胶质瘤细胞甲酰化肽受体(formylpeptide receptor，FPR)功能的影响及其意义。以培养的人恶性胶质瘤细胞U87为研究对象，用FPR激动剂fMLF(n-formyl-methionyl-leucyl-phenylalanine)刺激细胞，以双室跨膜迁移模型检测细胞的迁移能力、计数法测定细胞的增殖能力、分光光度法测定细胞内钙流、RT-PCR方法测定血管内皮生长因子(vascular endothelial growth factor, VEGF)mRNA表达，以ELISA方法检测VEGF蛋白水平，并测定诺帝(25～100 μmol·L^-1)处理瘤细胞后上述功能指标的变化。50 μmol·L^-1诺帝能有效抑制fMLF诱导的细胞增殖、迁移(P<0.05)和细胞内钙流，100 μmol·L^-1诺帝能抑制VEGF mRNA表达，降低VEGF水平(P<0.05)。诺帝能抑制FPR介导的人恶性胶质瘤细胞增殖、迁移和VEGF产生，提示其具有抗肿瘤活性。

Effect of nordy on FPR function of malignant human glioma cell line U87

Nordy is a synthesized chrial compound. To investigate the effects of nordy (25 - 100 micromol x L(-1)) on the function of formylpeptide receptor (FPR) of malignant human glioma cells, human glioblastoma cell line U87 was used to detect its proliferation, migration, calcium mobilization, vascular endothelial growth factor (VEGF) mRNA and protein levels after activation of FPR by its agonist N-formyl-methionyl-leucyl-phenylalanine (fMLF). Cell proliferation, migration ability, VEGF mRNA, VEGF protein and calcium mobilization were evaluated by cell counting, chemotaxis assay, RT-PCR, ELISA and spectrometry. Nordy (50 - 100 micromol x L(-1)) potently inhibited the proliferation, migration and calcium mobilization of U87 cells induced by fMLF (P < 0.05). Moreover, 100 micromol x L(-1) nordy showed a significantly impaired VEGF mRNA expression and protein secretion induced by fMLF (P < 0.05). Nordy could inhibit FPR functioning in glioma cell proliferation, migration and angiogenesis, which might be a possible mechanism of its anti-cancer effects.