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本文引用的文献

1
Effect of lecithin in the treatment of ethanol mediated free radical induced hepatotoxicity.卵磷脂在治疗乙醇介导的自由基诱导的肝毒性中的作用。
Indian J Clin Biochem. 2006 Mar;21(1):62-9. doi: 10.1007/BF02913068.
2
Effect of ethanol on liver antioxidant defense systems: Adose dependent study.乙醇对肝脏抗氧化防御系统的影响:剂量依赖性研究。
Indian J Clin Biochem. 2005 Jan;20(1):80-4. doi: 10.1007/BF02893047.
3
An opium alkaloid-papaverine ameliorates ethanol-induced hepatotoxicity: Diminution of oxidative stress.一种鸦片生物碱——罂粟碱可改善乙醇诱导的肝毒性:减轻氧化应激。
Indian J Clin Biochem. 2000 Jul;15(2):155-60. doi: 10.1007/BF02883745.
4
Fenugreek (Trigonella foenum graecum) seed extract prevents ethanol-induced toxicity and apoptosis in Chang liver cells.胡芦巴(Trigonella foenum graecum)种子提取物可预防乙醇诱导的Chang肝细胞毒性和凋亡。
Alcohol Alcohol. 2006 May-Jun;41(3):267-73. doi: 10.1093/alcalc/agl020. Epub 2006 Mar 30.
5
Chronic ethanol consumption decreases mitochondrial and glycolytic production of ATP in liver.长期摄入乙醇会降低肝脏中ATP的线粒体和糖酵解生成量。
Alcohol Alcohol. 2006 May-Jun;41(3):254-60. doi: 10.1093/alcalc/agl017. Epub 2006 Mar 29.
6
Chemistry and hepatoprotective activity of an active fraction from Barleria prionitis Linn. in experimental animals.假杜鹃活性部位的化学性质及其在实验动物中的保肝活性
Phytother Res. 2005 May;19(5):391-404. doi: 10.1002/ptr.1509.
7
Alcohol, oxidative stress, and free radical damage.酒精、氧化应激与自由基损伤。
Alcohol Res Health. 2003;27(4):277-84.
8
Genetic polymorphism in ethanol metabolism: acetaldehyde contribution to alcohol abuse and alcoholism.乙醇代谢中的基因多态性:乙醛在酒精滥用和酒精中毒中的作用。
Mol Psychiatry. 2004 Jun;9(6):570-81. doi: 10.1038/sj.mp.4001497.
9
Effect of Piper betle leaf extract on alcoholic toxicity in the rat brain.蒌叶提取物对大鼠脑酒精毒性的影响。
J Med Food. 2003 Fall;6(3):261-5. doi: 10.1089/10966200360716689.
10
Activity of Cassia auriculata leaf extract in rats with alcoholic liver injury.决明叶提取物对酒精性肝损伤大鼠的作用
J Nutr Biochem. 2003 Aug;14(8):452-8. doi: 10.1016/s0955-2863(03)00053-6.

毛叶枣叶提取物对大鼠肝脏慢性乙醇诱导的肝毒性的抗氧化作用评估。

Evaluation of the antioxidant effects of Ziziphus mauritiana Lam. Leaf extracts against chronic ethanol-induced hepatotoxicity in rat liver.

作者信息

Dahiru D, Obidoa O

机构信息

Department of Biochemistry, Federal University of Technology, Yola P.M.B. 2076 Yola, Adamawa State, Nigeria. v

出版信息

Afr J Tradit Complement Altern Med. 2007 Oct 27;5(1):39-45. doi: 10.4314/ajtcam.v5i1.31254.

DOI:10.4314/ajtcam.v5i1.31254
PMID:20162053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2816599/
Abstract

Chronic alcohol ingestion is known to increase the generation of reactive oxygen species (ROS), thereby leading to liver damage. Antioxidant enzymes act individually or in combination to reduce or counter the effect of these ROS. Chronic administration of alcohol at (40% v/v, 1 ml/100 g), for 6 weeks showed a significant (p<0.05) elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TB). There was also a significant (p<0.05) decreased levels of catalase, glutathione peroxidase, glutathione reductase and superoxide dismutase compared to control rats. Pre-treatment of rats with 200, 400 mg/kg body weight of aqueous leaf extract of Ziziphus mauritiana or 100 mg/kg silymarin resulted in a significant (p<0.05) decreased levels of ALT, AST, ALP, and TB with levels of catalase, glutathione peroxidase, glutathione reductase and superoxide dismutase showing a significant (p<0.05) increase compared to group administered alcohol only. Histopathology of rat liver administered with alcohol only resulted in severe necrosis, mononuclear cell aggregation and fatty degeneration in the central and mid zonal areas which was a characteristic of a damaged liver. Pre-treatment with the aqueous extract of Ziziphus mauritiana or silymarin reduced the morphological changes that are associated with chronic alcohol administration. The presence of tannins, saponins and phenolic compounds observed in the plant extract could be responsible for the observed effects of decreasing the levels of injured tissue marker and lipid peroxidation.

摘要

已知长期摄入酒精会增加活性氧(ROS)的生成,从而导致肝损伤。抗氧化酶单独或联合发挥作用,以减少或对抗这些ROS的影响。以40%(体积/体积)、1毫升/100克的剂量对大鼠进行6周的酒精慢性给药后,丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和总胆红素(TB)水平显著升高(p<0.05)。与对照大鼠相比,过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和超氧化物歧化酶的水平也显著降低(p<0.05)。用200、400毫克/千克体重的毛里求斯枣树叶水提取物或100毫克/千克水飞蓟宾对大鼠进行预处理,导致ALT、AST、ALP和TB水平显著降低(p<0.05),而过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和超氧化物歧化酶的水平与仅给予酒精的组相比显著升高(p<0.05)。仅给予酒精的大鼠肝脏组织病理学检查显示,中央和中区出现严重坏死、单核细胞聚集和脂肪变性,这是肝脏受损的特征。用毛里求斯枣树叶水提取物或水飞蓟宾进行预处理可减少与长期酒精给药相关的形态学变化。植物提取物中观察到的单宁、皂苷和酚类化合物可能是观察到的降低损伤组织标志物水平和脂质过氧化作用的原因。