Department of Pharmacology, School of Pharmacy, University of Seville, C/Profesor Garcia Gonzalez no2, 41012, Seville, Spain.
Curr Pharm Des. 2012;18(26):3939-65. doi: 10.2174/138161212802083725.
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder caused by deregulated immune responses in a genetically predisposed individual. This is a complex process mediated by cytokines, chemokines, adhesion molecules, cytoplasm nuclear receptors, among others. Recent data support a participation of the endoplasmic reticulum (ER) stress and mitochondrial dysfunctions in IBD. Moreover, now it is evident that chronic degenerative pathologies, including IBD, share comparable disease mechanisms at the cellular level with alteration of the autophagy mechanisms. Mounting evidence suggests that the risk of developing colorectal cancer (CRC) is dramatically increased in patients with chronic inflammatory disease. Chronic inflammation in IBD exposes these patients to a number of signals known to have tumorigenic effects including nuclear factor kappa B (NF-κB) activation, proinflammatory cytokines and prostaglandins release and reactive oxygen species (ROS) production. Chemoprevention consists in the use of drugs, vitamins, or nutritional supplements to reduce the risk of developing, or having a recurrence of cancer. Numerous in vitro and animal studies have established the potential colon cancer chemopreventive properties of phytochemicals derived from both plants (curcumin, resveratrol, epigallocatechin gallate, quercetin or genistein) and substances from marine environment, including microalgae species and their products. This review summarizes the mechanisms by which these naturally occurring compounds may mediate chemopreventive effects on cancer. These actions include induction of cell cycle arrest and apoptosis, inhibition of cell proliferation, stimulation of antimetastatic and antiangiogenic responses and increased antioxidant and anti-inflammatory activity.
炎症性肠病（IBD）是一种由遗传易感性个体中免疫反应失调引起的慢性炎症性疾病。这是一个由细胞因子、趋化因子、黏附分子、细胞质核受体等介导的复杂过程。最近的数据支持内质网（ER）应激和线粒体功能障碍在 IBD 中的参与。此外，现在显然慢性退行性病变，包括 IBD，在细胞水平上与自噬机制的改变具有相似的疾病机制。越来越多的证据表明，患有慢性炎症性疾病的患者患结直肠癌（CRC）的风险显著增加。IBD 中的慢性炎症使这些患者暴露于许多已知具有致癌作用的信号，包括核因子 kappa B（NF-κB）激活、促炎细胞因子和前列腺素释放以及活性氧（ROS）产生。化学预防是指使用药物、维生素或营养补充剂来降低患癌症或癌症复发的风险。大量的体外和动物研究已经确立了来自植物（姜黄素、白藜芦醇、表没食子儿茶素没食子酸酯、槲皮素或染料木黄酮）和海洋环境（包括微藻物种及其产物）的植物化学物质对结肠癌的潜在化学预防作用。本文综述了这些天然化合物可能通过哪些机制介导对癌症的化学预防作用。这些作用包括诱导细胞周期停滞和细胞凋亡、抑制细胞增殖、刺激抗转移和抗血管生成反应以及增加抗氧化和抗炎活性。
