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肥胖状态下的炎症和氧化应激及没食子酸的保护作用。

Inflammation and Oxidative Stress in an Obese State and the Protective Effects of Gallic Acid.

机构信息

Department of Life and Environmental Sciences, Polytechnic University of Marche, 60131 Ancona, Italy.

Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg 7505, South Africa.

出版信息

Nutrients. 2018 Dec 21;11(1):23. doi: 10.3390/nu11010023.

DOI:10.3390/nu11010023
PMID:30577684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6356415/
Abstract

Metabolic complications in an obese state can be aggravated by an abnormal inflammatory response and enhanced production of reactive oxygen species. Pro-inflammatory response is known to be associated with the formation of toxic reactive oxygen species and subsequent generation of oxidative stress. Indeed, adipocytes from obese individuals display an altered adipokine profile, with upregulated expression and secretion of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin (IL-6). Interestingly, natural compounds, including phenolic enriched foods are increasingly explored for their ameliorative effects against various metabolic diseases. Of interest is gallic acid, a trihydroxybenzoic acid that has progressively demonstrated robust anti-obesity capabilities in various experimental models. In addition to reducing excessive lipid storage in obese subjects, gallic acid has been shown to specifically target the adipose tissue to suppress lipogenesis, improve insulin signaling, and concomitantly combat raised pro-inflammatory response and oxidative stress. This review will revise mechanisms involved in the pathophysiological effects of inflammation and oxidative stress in an obese state. To better inform on its therapeutic potential and improvement of human health, available evidence reporting on the anti-obesity properties of gallic acid and its derivatives will be discussed, with emphases on its modulatory effect on molecular mechanisms involved in insulin signaling, inflammation and oxidative stress.

摘要

肥胖状态下的代谢并发症可能会因异常的炎症反应和活性氧物质的产生而加重。已知促炎反应与有毒活性氧物质的形成以及随后的氧化应激有关。事实上,肥胖个体的脂肪细胞表现出改变的脂肪因子谱,上调表达和分泌促炎细胞因子,如肿瘤坏死因子-α (TNF-α) 和白细胞介素 (IL-6)。有趣的是,包括富含酚类的食物在内的天然化合物因其对各种代谢疾病的改善作用而越来越受到关注。值得注意的是,没食子酸是一种三羟基苯甲酸,在各种实验模型中已逐渐证明具有强大的抗肥胖能力。除了减少肥胖患者过多的脂质储存外,没食子酸还被证明可以专门针对脂肪组织,抑制脂肪生成,改善胰岛素信号,并同时对抗升高的促炎反应和氧化应激。这篇综述将复习肥胖状态下炎症和氧化应激的病理生理作用涉及的机制。为了更好地了解其治疗潜力和改善人类健康,将讨论关于没食子酸及其衍生物的抗肥胖特性的现有证据,并强调其对涉及胰岛素信号、炎症和氧化应激的分子机制的调节作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/500f3c001d24/nutrients-11-00023-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/f9a85a9d8328/nutrients-11-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/261e2dd0b824/nutrients-11-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/f3dd3d22781a/nutrients-11-00023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/500f3c001d24/nutrients-11-00023-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/f9a85a9d8328/nutrients-11-00023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/261e2dd0b824/nutrients-11-00023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/f3dd3d22781a/nutrients-11-00023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0c5/6356415/500f3c001d24/nutrients-11-00023-g004.jpg

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