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本文引用的文献

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Pathogenesis and management of alcoholic liver cirrhosis: a review.酒精性肝硬化的发病机制与管理:综述
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2
CYP2E1 potentiates binge alcohol-induced gut leakiness, steatohepatitis, and apoptosis.细胞色素P450 2E1增强暴饮酒精诱导的肠道通透性增加、脂肪性肝炎和细胞凋亡。
Free Radic Biol Med. 2013 Dec;65:1238-1245. doi: 10.1016/j.freeradbiomed.2013.09.009. Epub 2013 Sep 21.
3
Differential activation of catalase expression and activity by PPAR agonists: implications for astrocyte protection in anti-glioma therapy.过氧化物酶体增殖物激活受体激动剂对过氧化氢酶表达和活性的差异激活:对抗胶质瘤治疗中星形胶质细胞保护的意义。
Redox Biol. 2013 Jan 26;1(1):70-9. doi: 10.1016/j.redox.2012.12.006. eCollection 2013.
4
Fenofibrate suppresses melanogenesis in B16-F10 melanoma cells via activation of the p38 mitogen-activated protein kinase pathway.非诺贝特通过激活 p38 丝裂原活化蛋白激酶通路抑制 B16-F10 黑素瘤细胞的黑色素生成。
Chem Biol Interact. 2013 Oct 5;205(3):157-64. doi: 10.1016/j.cbi.2013.07.008. Epub 2013 Jul 18.
5
Alcoholic liver disease and pancreatitis: global health problems being addressed by the US National Institute on Alcohol Abuse and Alcoholism.酒精性肝病和胰腺炎:美国国家酒精滥用和酒精中毒研究所解决的全球健康问题。
J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1:4-6. doi: 10.1111/jgh.12246.
6
Peroxisome-proliferator-activated receptors regulate redox signaling in the cardiovascular system.过氧化物酶体增殖物激活受体调节心血管系统中的氧化还原信号传导。
World J Cardiol. 2013 Jun 26;5(6):164-74. doi: 10.4330/wjc.v5.i6.164.
7
Role of oxidative stress in the pathogenesis of alcohol-induced liver disease.氧化应激在酒精性肝病发病机制中的作用。
Free Radic Res. 2013 Nov;47(11):894-904. doi: 10.3109/10715762.2013.819428. Epub 2013 Oct 4.
8
Ethanol metabolism and oxidative stress are required for unfolded protein response activation and steatosis in zebrafish with alcoholic liver disease.乙醇代谢和氧化应激是激活斑马鱼酒精性肝病未折叠蛋白反应和脂肪变性所必需的。
Dis Model Mech. 2013 Sep;6(5):1213-26. doi: 10.1242/dmm.012195. Epub 2013 Jun 20.
9
Activation of peroxisome proliferator activated receptor alpha ameliorates ethanol mediated liver fibrosis in mice.过氧化物酶体增殖物激活受体α的激活可改善乙醇诱导的小鼠肝纤维化。
Lipids Health Dis. 2013 Feb 6;12:11. doi: 10.1186/1476-511X-12-11.
10
Interleukin-10 gene modification attenuates hepatocyte activation of rat hepatic stellate cells in vitro.白细胞介素-10 基因修饰可减轻大鼠肝星状细胞在体外的肝细胞激活。
Mol Med Rep. 2013 Feb;7(2):371-8. doi: 10.3892/mmr.2012.1228. Epub 2012 Dec 11.

过氧化物酶体增殖物激活受体α,酒精性肝病的一个潜在治疗靶点。

Peroxisome proliferator-activated receptor α, a potential therapeutic target for alcoholic liver disease.

作者信息

Nan Yue-Min, Wang Rong-Qi, Fu Na

机构信息

Yue-Min Nan, Rong-Qi Wang, Na Fu, Department of Traditional and Western Medical Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang 050051, Hebei Province, China.

出版信息

World J Gastroenterol. 2014 Jul 7;20(25):8055-60. doi: 10.3748/wjg.v20.i25.8055.

DOI:10.3748/wjg.v20.i25.8055
PMID:25009377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4081676/
Abstract

Alcoholic liver injury represents a progressive process with a range of consequences including hepatic steatosis, steatohepatitis, liver fibrosis, cirrhosis, and hepatocellular carcinoma. Targeting key molecular regulators involved in the development of alcoholic liver injury may be of great value in the prevention of liver injury. Peroxisome proliferator-activated receptor α (PPARα) plays a pivotal role in modulation of hepatic lipid metabolism, oxidative stress, inflammatory response and fibrogenesis. As such, PPARα may be a potential therapeutic target for the treatment of alcoholic liver disease.

摘要

酒精性肝损伤是一个渐进的过程,会产生一系列后果,包括肝脂肪变性、脂肪性肝炎、肝纤维化、肝硬化和肝细胞癌。针对参与酒精性肝损伤发展的关键分子调节因子,可能对预防肝损伤具有重要价值。过氧化物酶体增殖物激活受体α(PPARα)在调节肝脏脂质代谢、氧化应激、炎症反应和纤维生成中起关键作用。因此,PPARα可能是治疗酒精性肝病的一个潜在治疗靶点。