摘要
背景:粘膜屏障功能缺陷是导致许多人类炎症性肠道疾病不受控制的发病和发展的主要原因,这些疾病的主要特征是慢性炎症性肠病(Chr)。ONIC间歇性免疫和炎症反应导致肠道结构损害,这可能是结直肠癌发展的潜在危险。 在活动性疾病期,主要表现为促炎细胞因子和趋化因子的产生,以及活化的白细胞和上皮细胞的氧化反应。肠道炎症。 目的:氧化应激在肠损伤的发生发展中起着关键作用。事实上,活性氧及其氧化副产物对氧化还原敏感信号通路和Tran有调节作用。粘附因子,维持肠道层内的炎症。 方法:多不饱和脂肪酸和胆固醇是氧化修饰的主要靶点。 这些脂类是细胞膜成分或存在于食品中,容易经过非酶氧化而形成化学反应物种,从而产生广泛的生物效应。s包括炎症、程序性细胞死亡和增殖。 结果与结论:本文综述了脂质氧化产物在调节氧化还原途径中的作用及其在炎症相关GU发病机制中的作用。T病。特别是考虑到脂质过氧化终产物,如异脯氨酸和醛,以及胆固醇氧化衍生的草酸醇。 在饮食中使用特定的抗氧化剂和抗炎分子来控制氧化损伤和组织局部过度产生脂质氧化产物可能具有临床意义。d治疗效益。
关键词: 肠道,肠道疾病,丙烯醛,异前列腺素,4-羟基壬醛,丙二醛,草酸,多酚。
Current Medicinal Chemistry
Title:Lipid Oxidation Products in the Pathogenesis of Inflammation-related Gut Diseases
Volume: 25 Issue: 11
关键词: 肠道,肠道疾病,丙烯醛,异前列腺素,4-羟基壬醛,丙二醛,草酸,多酚。
摘要: Background: A defective mucosal barrier function is the principal cause of the uncontrolled onset and progression of a number of human inflammatory gut diseases, most of which are characterized by chronic intermittent immune and inflammatory responses leading to structural intestinal damage, which can represent a potential risk for colorectal cancer development.
During the active disease phase the production of pro-inflammatory cytokines and chemokines, and the induction of oxidative reactions by activated leukocytes and epithelial cells represent the main event in the intestinal inflammation.
Objective: Oxidative stress plays a key role in the development of intestinal damage. Indeed reactive oxygen species and their oxidized by-products regulate redox-sensitive signaling pathways and transcription factors, which sustain inflammation within the intestinal layer.
Methods: Polyunsaturated fatty acids and cholesterol are the principal targets of oxidative modifications.
These lipids, which are cell membrane constituents or are present in food, readily undergo non-enzymatic oxidation to form chemically-reactive species that can induce a wide range of biological effects including inflammation, programmed cell death, and proliferation.
Results and Conclusions: In this review we summarize the current knowledge on the role of lipid oxidation products in regulating redox pathways involved in the pathogenesis of inflammation- related gut diseases. In particular, lipid peroxidation end products, such as isoprostanes and aldehydes, and cholesterol oxidation-derived oxysterols are taken into consideration.
The control of oxidative damage and consequently tissue local over-production of lipid oxidation products by using specific antioxidant and anti-inflammatory molecules in the diet may have clinical and therapeutic benefits.
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Cite this article as:
Lipid Oxidation Products in the Pathogenesis of Inflammation-related Gut Diseases, Current Medicinal Chemistry 2018; 25 (11) . https://dx.doi.org/10.2174/0929867324666170619104105
DOI https://dx.doi.org/10.2174/0929867324666170619104105 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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