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首页> 外文期刊>Cancer prevention research. >American Ginseng Attenuates Colitis-Associated Colon Carcinogenesis in Mice: Impact on Gut Microbiota and Metabolomics
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American Ginseng Attenuates Colitis-Associated Colon Carcinogenesis in Mice: Impact on Gut Microbiota and Metabolomics

机译：花旗参可减轻小鼠结肠炎相关结肠癌的发生：对肠道菌群和代谢组学的影响

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Inflammatory bowel disease is a risk factor for colorectal cancer initiation and development. In this study, the effects of American ginseng on chemically induced colitis and colon carcinogenesis were evaluated using an azoxymethane (AOM)/dextran sulfate sodium (DSS) mouse model. During the acute phase on day 15, the oral administration of ginseng (15 and 30 mg/kg/day) significantly suppressed AOM/DSS-induced colitis, as demonstrated by the disease activity index and colon tissue histology. During the chronic phase in week 13, AOM/DSS-induced tumor multiplicity was significantly suppressed by ginseng. Ginseng significantly attenuated the increase of inflammatory cytokines, such as IL1 alpha, IL1 beta, IL6, G-CSF, and GM-CSF. Serum metabolomics data in the PCA plots showed good separation between the AOM/DSS model and ginseng-treated mice, and the most important endogenous metabolite changes were identified. The 16S rRNA data showed that after AOM/DSS, the microbiome community in the model group was obviously changed, and ginseng inhibited these changes. Fecal metabolomics analysis supported these findings. In conclusion, oral ginseng significantly decreased AOM/DSS-induced colitis and colon carcinogenesis by inhibiting inflammatory cytokines and restoring the metabolomics and microbiota profiles accordingly. Selective endogenous small molecules could be used as biomarkers to elucidate the effects of ginseng treatment. (C) 2016 AACR.
机译：肠炎是大肠癌发生和发展的危险因素。在这项研究中，西洋参对一种化学诱导的结肠炎和结肠癌发生的作用使用一种乙氧基甲烷（AOM）/右旋糖酐硫酸钠（DSS）小鼠模型进行了评估。在第15天的急性期，口服人参（15和30 mg / kg /天）可显着抑制AOM / DSS诱导的结肠炎，如疾病活动指数和结肠组织组织学所证明。在第13周的慢性阶段，人参可显着抑制AOM / DSS诱导的肿瘤多样性。人参显着减弱了炎症细胞因子（例如IL1 alpha，IL1 beta，IL6，G-CSF和GM-CSF）的增加。 PCA图中的血清代谢组学数据显示，AOM / DSS模型与人参治疗的小鼠之间具有良好的分离，并且鉴定出最重要的内源性代谢物变化。 16S rRNA数据显示，AOM / DSS后，模型组中的微生物组群落发生了明显变化，而人参则抑制了这些变化。粪便代谢组学分析支持了这些发现。总之，口服人参可通过抑制炎症细胞因子并相应地恢复代谢组学和微生物区系来显着降低AOM / DSS诱导的结肠炎和结肠癌的发生。选择性内源性小分子可用作生物标记物，以阐明人参治疗的效果。 （C）2016 AACR。

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