The protective effect of the M. calabura Linn. fruit ethanolic extract (MFEE) against nickel (Ni)-induced vascular endothelial growth factor (VEGF) expression in hepatocellular carcinoma (HepG2) cells was investigated. MFEE contained 4 flavonoids: epicatechin, rutin, diosmin and luteolin, and 11 phenolic acids: gallic acid, gentisic acid, p-hydroxybenzoic acid, vanillic acid, p-coumaric acid, ferulic acid, sinapic acid, syringic acid, p-anisic acid and rosmarinic acid. Substantial VEGF expression was assayed in Ni-stimulated HepG2 cells, which was significantly suppressed through MFEE treatment via down-regulating Raf-1 proto-oncogene, serine/threonine kinase (RAF1) /mitogen-activated protein kinase 1/2 (MEK1/2)/extracellular-signal-regulated kinase 1/2 (ERK1/2), and Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) pathways as well as inhibiting hypoxia-inducible factor (HIF)-1α expression down-regulated by phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. The results showed that MFEE should have the potential to lower liver cancer risk in the Ni-polluted environment by suppressing VEGF expression.

M. calabura Linn的保护作用。研究了水果乙醇提取物（MFEE）对镍（Ni）诱导的肝癌细胞（HepG2）细胞中血管内皮生长因子（VEGF）表达的影响。MFEE含有4种类黄酮：表儿茶素，芦丁，薯di和木犀草素，以及11种酚酸：没食子酸，龙胆酸，对羟基苯甲酸，香草酸，对香豆酸，阿魏酸，芥子酸，丁香酸，p-茴香酸和迷迭香酸。在Ni刺激的HepG2细胞中检测到大量的VEGF表达，通过下调Raf-1原癌基因，丝氨酸/苏氨酸激酶（RAF1）/丝裂原激活的蛋白激酶1/2（MEK1 / 2），通过MFEE处理可显着抑制VEGF的表达。 ）/细胞外信号调节激酶1/2（ERK1 / 2）和Janus激酶2（JAK2）/信号转导子和转录激活子3（STAT3）途径以及抑制缺氧诱导因子（HIF）-1α的表达被磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（AKT）/哺乳动物雷帕霉素靶标（mTOR）途径下调。结果表明，MFEE应该具有通过抑制VEGF表达来降低镍污染环境中肝癌风险的潜力。