Polyphenols-rich extract from Pleurotus eryngii with growth inhibitory of HCT116 colon cancer cells and anti-inflammatory function in RAW264.7 cells
Polyphenols-rich extract from Pleurotus eryngii with growth inhibitory of HCT116 colon cancer cells and anti-inflammatory function in RAW264.7 cells
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富含多酚的杏鲍菇提取物对 HCT116 结肠癌细胞生长具有抑制作用，并对 RAW264.7 细胞具有抗炎作用
DOI：
10.1039/c7fo01794d
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发表时间：
2018-03-01
期刊：
影响因子：
6.1
通讯作者：
Yang, Wenjian
中科院分区：
文献类型：
--
作者：
Hu, Qiuhui;Yuan, Biao;Yang, Wenjian
食用菌是生物活性成分的丰富来源。本研究从一种食用菌中分离得到一种富含多酚的提取物，命名为PPEP。采用超高效液相色谱-三重飞行时间质谱联用技术（UPLC-TOF/MS/MS），从PPEP中鉴定出没食子酸一水合物、3-（3，4-二羟基苯基）-丙酸、没食子酸甲酯、胡萝卜酸、鞣花酸和儿茶素。这种富含酚类的提取物PPEP通过抑制促炎介质包括一氧化氮（NO）和活性氧（ROS）的过度产生而在脂多糖刺激的RAW 264. 7巨噬细胞中表现出抗炎作用。PPEP的抗炎作用与抑制iNOS表达、抑制p-I κ B蛋白表达、抑制NE κ B和l κ B mRNA表达有关。接下来，还测定了PPEP对人结肠癌细胞的抑制效果。PPEP以剂量和时间依赖的方式抑制人结肠癌HCT 116细胞的细胞增殖，而在相同的测试浓度（0-200 μ g mL（-1））下，它对正常人结肠肌成纤维细胞CCD-18 Co细胞没有抑制作用。此外，PPEP诱导人结肠癌细胞周期阻滞并导致广泛的细胞凋亡，这与下调细胞周期相关信号蛋白如cyclin B和cyclin E，上调凋亡相关信号蛋白caspase-3和cleaved caspase-3有关。总的来说，我们的研究结果提供了一个基础，使用PPEP作为一个有前途的预防剂对炎症性疾病和结肠癌。
Edible mushrooms are rich sources of bioactive components. In this study, a polyphenol-rich extract, designated as PPEP, was isolated from an edible mushroom, Pleurotus eryngii. Using ultra high performance liquid chromatograph combined with triple time-of-flight mass spectrometry (UPLC-TOF/MS/MS), gallic acid monohydrate, 3-(3,4-dihydroxyphenyl)-propionic acid, methyl gallate, syringic acid, ellagic acid and catechin were identified in PPEP. This phenolic-rich extract PPEP exhibited anti-inflammatory effect in lipopolysaccharide-stimulated RAW264.7 macrophages by inhibiting the overproduction of pro-inflammatory mediators including nitric oxide (NO) and reactive oxygen species (ROS). It was demonstrated that the anti-inflammatory effects of PPEP were associated with the inhibition of iNOS expression, suppression of p-I kappa B protein expression and inhibition of NE-kappa B and l kappa B mRNA expression. Next, the inhibitory effect of PPEP against human colon cancer cells was also determined. PPEP suppressed cell proliferation of human colon cancer HCT116 cells in a dose-and time-dependent fashion, while it showed no inhibitory effect on normal human colonic myofibroblasts CCD-18Co cells at the same tested concentrations (0-200 mu g mL(-1)). Moreover, PPEP induced cell cycle arrest and led to extensive cellular apoptosis in human colon cancer cells, which was associated with the downregulation of cell cycle-related signaling protein, e.g. cyclin B and cyclin E, and the upregulation of apoptosis-related signaling protein caspase-3 and cleaved caspase-3. Overall, our results provided a basis for using PPEP as a promising preventive agent against inflammatory disease and colon cancer.