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姜黄素改善 2 型糖尿病肝纤维化——对其作用机制的深入了解。

Curcumin ameliorates hepatic fibrosis in type 2 diabetes mellitus - insights into its mechanisms of action.

机构信息

Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.

出版信息

Br J Pharmacol. 2012 Aug;166(8):2209-11. doi: 10.1111/j.1476-5381.2012.01959.x.

DOI:10.1111/j.1476-5381.2012.01959.x
PMID:22452372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3448887/
Abstract

UNLABELLED

A wide variety of beneficial effects have been attributed to curcumin, a major polyphenol from the golden spice Curcuma longa known as turmeric, including amelioration of severe complications of type 2 diabetes such as hepatic fibrosis, retinopathy, neuropathy and nephropathy. In the present issue of BJP, Lin and colleagues reveal new mechanisms by which curcumin inhibits the activation of hepatic stellate cells in vitro, a hallmark of non-alcoholic steatohepatitis and hepatic fibrogenesis associated with type 2 diabetes mellitus. They demonstrated that curcumin suppresses the advanced glycation end-products (AGEs)-mediated induction of the receptor for AGEs (RAGE) gene expression by increasing PPARγ activity and stimulating de novo synthesis of glutathione. As a result, downstream elements of RAGE-activated pathways are inhibited, which prevents oxidative stress, inflammation and hepatic stellate cell activation. This report suggests that curcumin may have potential as an anti-fibrotic agent in type 2 diabetes and opens the door to the evaluation of curcumin therapeutic effects in liver conditions of different aetiology and in other disorders linked to the impairment of PPARγ activity, such as obesity and atherosclerosis.

LINKED ARTICLE

This article is a commentary on Lin et al., pp. 2212-2227 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2012.01910.x.

摘要

未加标签

姜黄,一种来自姜黄的主要多酚,被称为 turmeric,具有多种有益作用,包括改善 2 型糖尿病的严重并发症,如肝纤维化、视网膜病变、神经病变和肾病。在 BJP 的本期中,Lin 及其同事揭示了姜黄抑制体外肝星状细胞激活的新机制,肝星状细胞激活是与 2 型糖尿病相关的非酒精性脂肪性肝炎和肝纤维化的标志。他们表明,姜黄通过增加 PPARγ 活性和刺激谷胱甘肽的从头合成来抑制晚期糖基化终产物 (AGEs)介导的 AGEs 受体 (RAGE)基因表达的诱导。因此,RAGE 激活途径的下游元件被抑制,从而防止氧化应激、炎症和肝星状细胞激活。该报告表明,姜黄可能具有作为 2 型糖尿病抗纤维化剂的潜力,并为评估姜黄在不同病因的肝脏疾病和与 PPARγ 活性受损相关的其他疾病(如肥胖和动脉粥样硬化)中的治疗效果开辟了道路。

相关文章

本文是 Lin 等人在本期杂志第 2212-2227 页上的评论文章。要查看本文,请访问 http://dx.doi.org/10.1111/j.1476-5381.2012.01910.x。

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本文引用的文献

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Curcumin inhibits gene expression of receptor for advanced glycation end-products (RAGE) in hepatic stellate cells in vitro by elevating PPARγ activity and attenuating oxidative stress.姜黄素通过提高 PPARγ 活性和减轻氧化应激来抑制肝星状细胞中晚期糖基化终产物受体(RAGE)的基因表达。
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2
Challenges associated with curcumin therapy in Alzheimer disease.与阿尔茨海默病中姜黄素治疗相关的挑战。
Expert Rev Mol Med. 2011 Nov 4;13:e34. doi: 10.1017/S1462399411002055.
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Amelioration of renal ischaemia-reperfusion injury by liposomal delivery of curcumin to renal tubular epithelial and antigen-presenting cells.姜黄素脂质体递送至肾小管上皮细胞和抗原提呈细胞减轻肾缺血再灌注损伤。
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Curcumin: an anti-inflammatory molecule from a curry spice on the path to cancer treatment.姜黄素:咖喱香料中的一种抗炎分子,有望成为癌症治疗的新途径。
Molecules. 2011 Jun 3;16(6):4567-98. doi: 10.3390/molecules16064567.
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Epigenetic silencing of peroxisome proliferator-activated receptor γ is a biomarker for colorectal cancer progression and adverse patients' outcome.过氧化物酶体增殖物激活受体 γ 的表观遗传沉默是结直肠癌进展和患者不良预后的生物标志物。
PLoS One. 2010 Dec 3;5(12):e14229. doi: 10.1371/journal.pone.0014229.
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Folia Biol (Praha). 2010;56(5):195-200.
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Curcumin prevents leptin raising glucose levels in hepatic stellate cells by blocking translocation of glucose transporter-4 and increasing glucokinase.姜黄素通过阻止葡萄糖转运蛋白-4的易位和增加葡萄糖激酶来防止瘦素升高肝星状细胞中的葡萄糖水平。
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