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本文引用的文献

1
The role of ethanol metabolism in development of alcoholic steatohepatitis in the rat.乙醇代谢在大鼠酒精性脂肪性肝炎发生发展中的作用。
Alcohol. 2010 Mar;44(2):157-69. doi: 10.1016/j.alcohol.2009.11.002. Epub 2010 Jan 29.
2
beta-Carotene exhibits antioxidant and anti-apoptotic properties to prevent ethanol-induced cytotoxicity in isolated rat hepatocytes.β-胡萝卜素具有抗氧化和抗细胞凋亡特性,可防止乙醇诱导的离体大鼠肝细胞毒性。
Phytother Res. 2010 Jun;24 Suppl 2:S183-9. doi: 10.1002/ptr.3068.
3
Effects of beta-carotene on antioxidant status in rats with chronic alcohol consumption.β-胡萝卜素对长期饮酒大鼠抗氧化状态的影响。
Cell Biochem Funct. 2009 Aug;27(6):344-50. doi: 10.1002/cbf.1579.
4
Alcohol metabolites and lipopolysaccharide: roles in the development and/or progression of alcoholic liver disease.酒精代谢产物与脂多糖:在酒精性肝病发生发展中的作用
World J Gastroenterol. 2009 Mar 14;15(10):1209-18. doi: 10.3748/wjg.15.1209.
5
Interactions of beta-carotene and flavonoids on the secretion of pro-inflammatory mediators in an in vitro system.β-胡萝卜素与类黄酮在体外系统中对促炎介质分泌的相互作用。
Chem Biol Interact. 2009 May 15;179(2-3):386-93. doi: 10.1016/j.cbi.2008.12.006. Epub 2008 Dec 16.
6
Carotenoids: actual knowledge on food sources, intakes, stability and bioavailability and their protective role in humans.类胡萝卜素:关于食物来源、摄入量、稳定性、生物利用度及其对人类保护作用的实际知识。
Mol Nutr Food Res. 2009 Sep;53 Suppl 2:S194-218. doi: 10.1002/mnfr.200800053.
7
[Hepatocyte oxidant stress and alcoholic liver disease].[肝细胞氧化应激与酒精性肝病]
Rev Esp Enferm Dig. 2008 Mar;100(3):156-63. doi: 10.4321/s1130-01082008000300006.
8
Oxidative mechanisms in the pathogenesis of alcoholic liver disease.酒精性肝病发病机制中的氧化机制。
Mol Aspects Med. 2008 Feb-Apr;29(1-2):9-16. doi: 10.1016/j.mam.2007.09.004. Epub 2007 Oct 7.
9
Lycopene and beta-carotene protect in vivo iron-induced oxidative stress damage in rat prostate.番茄红素和β-胡萝卜素可保护大鼠前列腺免受体内铁诱导的氧化应激损伤。
Braz J Med Biol Res. 2006 Feb;39(2):203-10. doi: 10.1590/s0100-879x2006000200006. Epub 2006 Feb 2.
10
Alcohol and oxidative liver injury.酒精与肝脏氧化损伤
Hepatology. 2006 Feb;43(2 Suppl 1):S63-74. doi: 10.1002/hep.20957.

不同剂量β-胡萝卜素对慢性乙醇喂养大鼠的抗凋亡作用。

The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats.

机构信息

School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan;

Department of Nutrition, I-Shou University, Kaohsiung, Taiwan;

出版信息

Hepatobiliary Surg Nutr. 2013 Jun;2(3):132-41. doi: 10.3978/j.issn.2304-3881.2013.06.08.

DOI:10.3978/j.issn.2304-3881.2013.06.08
PMID:24570931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3924668/
Abstract

BACKGROUND

Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.

METHODS

Rats were divided into 6 groups: C (control liquid diet), CLB [control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.

RESULTS

Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.

CONCLUSIONS

The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.

摘要

背景

乙醇摄入可能诱导肝凋亡并导致肝损伤。本研究旨在探讨不同剂量β-胡萝卜素补充对慢性乙醇喂养大鼠抗氧化能力和肝凋亡的影响。

方法

将大鼠分为 6 组:C(对照液体饮食)、CLB(对照液体饮食+β-胡萝卜素 0.52mg/kg 体重/天)、CHB(对照液体饮食+β-胡萝卜素 2.6mg/kg 体重/天)、E(乙醇液体饮食)、ELB(乙醇液体饮食+β-胡萝卜素 0.52mg/kg 体重/天)和 EHB(乙醇液体饮食+β-胡萝卜素 2.6mg/kg 体重/天)。12 周后处死大鼠,采集血液和肝脏样本进行分析。

结果

E 组大鼠的脂质过氧化和肝细胞色素 P4502E1(CYP2E1)表达增加,Fas 配体、caspase-8、细胞色素 c、caspase-9 和 -3 的表达明显增加。然而,ELB 组大鼠的脂质过氧化和 CYP2E1、caspase-9 和 -3 的表达明显降低,Bcl-xL 的表达明显升高。EHB 组大鼠的肿瘤坏死因子(TNF)-α水平、脂质过氧化和细胞色素 c 的表达明显降低,Bcl-2 的表达明显升高。

结论

这些结果表明,乙醇处理导致氧化应激和肝凋亡导致肝损伤,而β-胡萝卜素补充(0.52mg/kg 体重/天)可以通过降低乙醇诱导的氧化应激和抑制肝脏凋亡来预防乙醇引起的肝损伤。