Tectoridin, an isoflavone glycoside from the flower of Pueraria lobata, prevents acute ethanol-induced liver steatosis in mice
Tectoridin, an isoflavone glycoside from the flower of Pueraria lobata, prevents acute ethanol-induced liver steatosis in mice
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鸢尾素（一种来自葛根花的异黄酮糖苷）可预防小鼠急性乙醇诱导的肝脂肪变性
DOI：
10.1016/j.tox.2010.07.007
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发表时间：
2010-09-30
期刊：
影响因子：
4.5
通讯作者：
Wang, Zhengrong
中科院分区：
文献类型：
--
作者：
Xiong, Yu;Yang, Yuqing;Wang, Zhengrong
在传统中医中，葛根花（葛根花）被用于治疗与饮酒和肝损伤相关的问题。本研究主要研究了枇杷花的异黄酮苷——鸢尾苷的保肝作用及其机制。Ohwi。乙醇（5 g/kg）每12 h口服一次，共3次。末次给药后1 h，连续3天灌胃5次鸢尾苷（25、50、100 mg/kg）。给药后4 h处死小鼠。通过生化分析和实时定量聚合酶链反应（qPCR）对过氧化物酶体增殖物活化受体α (PPAR α)、甾醇调节元件结合蛋白(SREBP)-1c及其靶基因进行评价。分离线粒体进行线粒体通透性转移（MPT）和膜电位（δ Psi(m)）测定。急性乙醇暴露导致谷丙转氨酶（ALT）、天冬氨酸转氨酶（AST）和甘油三酯（TG）水平显著升高，肝脏线粒体功能紊乱，表现为MPT升高和δ Psi(m)降低。然而，tectoridin治疗显著减弱了这些影响。此外，鸢尾碱还能显著缓解硫代巴比妥酸反应物质的过量产生。此外，鸢尾素在mRNA和酶活性水平上抑制PPAR α及其靶基因(中链酰基辅酶a脱氢酶（MCAD）、酰基辅酶a氧化酶（ACO）和细胞色素P450 4A （CYP 4A）的表达。这些数据表明，鸢尾碱主要通过调节PPAR α通路的紊乱和改善线粒体功能来保护乙醇诱导的肝脏脂肪变性。2010爱思唯尔爱尔兰有限公司版权所有。
In traditional Chinese medicine, the flower of Pueraria lobata (Puerariae Flos) has been used in therapy to counteract the problems associated with alcohol drinking and liver injury. In this study, we investigated the hepatoprotective effects and its mechanisms of tectoridin, an isoflavone glycoside from the flower of P. lobata (Willd.) Ohwi. Ethanol (5 g/kg) was given orally every 12 h for a total of three doses. 1 h after the last dose of ethanol, tectoridin (25, 50 and 100 mg/kg) was given intragastrically five times in three consecutive days. The mice were sacrificed at 4 h after tectoridin treatment. Peroxisome proliferators-activated receptor alpha (PPAR alpha), sterol regulatory element-binding protein (SREBP)-1c and their target genes were evaluated by biochemical analysis and quantitative real-time polymerase chain reaction (qPCR). Mitochondria were isolated for the mitochondrial permeability transition (MPT) and membrane potential (Delta Psi(m)) assay. Acute ethanol exposure resulted in the significant increase of the alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglyceride (TG) levels and hepatic mitochondria dysfunction shown as the increase of MPT and the decrease of Delta Psi(m). However, tectoridin treatment dramatically attenuated these effects. In addition, tectoridin remarkably alleviated the over-production of thiobarbituric acid-reactive substance. Furthermore, tectoridin inhibited the decrease of PPAR alpha expression and its target genes, including medium-chain acyl-CoA dehydrogenase (MCAD), acyl-CoA oxidase (ACO) and cytochrome P450 4A (CYP 4A) at mRNA and enzyme activity levels. These data showed that tectoridin protected against ethanol-induced liver steatosis mainly through modulating the disturbance of PPAR alpha pathway and ameliorating mitochondrial function. (C) 2010 Elsevier Ireland Ltd. All rights reserved.