University of Connecticut, Storrs, Connecticut 06269-4017, USA.
Nutr Cancer. 2010;62(3):362-70. doi: 10.1080/01635580903407239.
Colorectal cancer (CRC) is a leading cause of cancer-related deaths in the United States. Epidemiological data have suggested that coffee consumption is inversely related to CRC risk, which may be attributed to chlorogenic acid (CGA), an ester of caffeic acid (CA) and quinic acid. This study was conducted to determine whether chronic dietary CGA supplementation would attenuate tumorigenesis and oxidative stress in a mouse model of azoxymethane (AOM)-induced colon cancer. Mice (4-wk old; n = 15/group) were fed CGA (0%, 0.01%, or 0.1%) for 20 wk and received 6 weekly intraperitoneal AOM injections (10 mg/kg). CGA and CA dose-dependently accumulated in the small intestinal mucosa. AOM induced (P < 0.05) colonic aberrant crypt foci (14.2 +/- 1.9/field) and tumors (14.6 +/- 1.1/colon), which were correlated (r = .677; P < 0.05), and CGA at either dose did not reduce tumorigenesis. Hepatic GSH/GSSG and Cys/CySS ratios were unaffected by AOM, but CGA at 0.1% increased these ratios by decreasing GSSG and CySS. CGA did not affect the ratios of small intestinal GSH/GSSG or Cys/CySS, which were decreased in response to AOM treatment. Collectively, these data indicated that CGA did not protect against AOM-induced tumorigenesis but affected hepatic thiol redox status in this colon cancer model.
结直肠癌（CRC）是美国癌症相关死亡的主要原因。流行病学数据表明，咖啡的消耗与 CRC 风险呈负相关，这可能归因于绿原酸（CGA），即咖啡酸（CA）和奎尼酸的酯。本研究旨在确定慢性饮食 CGA 补充是否会减弱氧化偶氮甲烷（AOM）诱导的结肠癌小鼠模型中的肿瘤发生和氧化应激。将小鼠（4 周龄；每组 n = 15）用 CGA（0%、0.01%或 0.1%）喂养 20 周，并接受 6 次每周腹腔内 AOM 注射（10mg/kg）。CGA 和 CA 呈剂量依赖性地积累在小肠黏膜中。AOM 诱导（P < 0.05）结肠异常隐窝病灶（14.2 +/- 1.9/视野）和肿瘤（14.6 +/- 1.1/结肠），这两者呈正相关（r =.677；P < 0.05），且任何剂量的 CGA 均不能降低肿瘤发生。AOM 对肝 GSH/GSSG 和 Cys/CySS 比值没有影响，但 0.1%的 CGA 通过降低 GSSG 和 CySS 增加了这些比值。CGA 对小肠 GSH/GSSG 或 Cys/CySS 的比值没有影响，AOM 处理降低了这些比值。总的来说，这些数据表明 CGA 不能预防 AOM 诱导的肿瘤发生，但会影响这种结肠癌模型中的肝硫醇氧化还原状态。
