Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, P.O. Box 12, 76100, Rehovot, Israel.
J Gastroenterol. 2012 May;47(5):504-18. doi: 10.1007/s00535-011-0514-7. Epub 2011 Dec 21.
We have recently demonstrated that polysaccharides from fruiting body extract (FBE) or mycelia extract (ME) of the edible mushroom Pleurotus pulmonarius exert antiproliferative effects in intestinal cells and an anti-inflammatory effect in a dextran sulfate sodium (DSS) mouse model of acute colitis. The aim of this study was to assess the role of fungal FBE and ME in colon carcinogenesis.
In vitro, human colorectal cancer cells were treated with FBE and ME and analyzed for inflammation response, for markers of apoptosis, and for cell-cycle progression. In vivo, FBE and ME were tested in a mouse model of colitis-associated colorectal carcinogenesis induced by cyclic treatments with DSS and azoxymethane. Treated mice were fed a daily diet containing 2 or 20 mg FBE or ME per mouse for 80 days.
In vitro, FBE and ME induced apoptosis in a dose-responsive manner and modulated the expression of Bcl-2, Bax, and cytochrome c, and blocked tumor necrosis factor (TNF)-α-induced inhibitor of nuclear factor (NF) (Iκ)-Bα degradation and NF-κB nuclear translocation. In vivo, dietary administration of FBE and ME significantly reduced the formation of aberrant crypt foci, which precedes colorectal cancer, and of microadenomas. The treatments significantly lowered the expression of proliferating cell nuclear antigen and increased the number of cells undergoing apoptosis in the colon. Additionally, FBE and ME inhibited the expression of the proinflammatory cytokine TNF-α in colonic tissue.
We conclude that P. pulmonarius FBE and ME inhibit colitis-associated colon carcinogenesis induced in mice through the modulation of cell proliferation, induction of apoptosis, and inhibition of inflammation.
我们最近证明，来自食用蘑菇肺形侧耳（Pleurotus pulmonarius）子实体提取物（FBE）或菌丝体提取物（ME）的多糖在肠细胞中具有抗增殖作用，并在葡聚糖硫酸钠（DSS）诱导的急性结肠炎小鼠模型中具有抗炎作用。本研究旨在评估真菌 FBE 和 ME 在结肠癌发生中的作用。
在体外，用 FBE 和 ME 处理人结直肠癌细胞，并分析炎症反应、凋亡标志物和细胞周期进程。在体内，用 FBE 和 ME 测试 DSS 和氧化偶氮甲烷循环处理诱导的结肠炎相关结直肠癌发生的小鼠模型。用含 2 或 20 毫克 FBE 或 ME 的每日饮食处理小鼠，持续 80 天。
在体外，FBE 和 ME 以剂量反应方式诱导细胞凋亡，并调节 Bcl-2、Bax 和细胞色素 c 的表达，并阻断肿瘤坏死因子（TNF）-α诱导的核因子（NF）-κB 抑制物（Iκ）-Bα降解和 NF-κB 核易位。在体内，饮食给予 FBE 和 ME 可显著减少结肠前期的异常隐窝灶和微腺瘤的形成。这些处理方法显著降低了增殖细胞核抗原的表达，并增加了结肠中正在进行凋亡的细胞数量。此外，FBE 和 ME 抑制了结肠组织中促炎细胞因子 TNF-α的表达。
我们得出结论，P. pulmonarius FBE 和 ME 通过调节细胞增殖、诱导细胞凋亡和抑制炎症来抑制小鼠诱导的结肠炎相关结肠癌的发生。
