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印度葛藤(Pueraria tuberosa)块根的肝毒性研究。

Hepatotoxicity of tubers of Indian Kudzu (Pueraria tuberosa) in rats.

机构信息

Department of Medicinal Chemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.

出版信息

Food Chem Toxicol. 2010 Apr;48(4):1066-71. doi: 10.1016/j.fct.2010.01.026. Epub 2010 Feb 1.

DOI:10.1016/j.fct.2010.01.026
PMID:20122980
Abstract

Methanolic extract of tubers of Pueraria tuberosa Linn. (Fabaceae) (PTME) has been tested for hepatoxicity in rats. In acute study, PTME (100-400 mg/100 g BW, given orally) showed LD(50) at 227.5 mg. For sub-chronic study, its repeated doses (5-100 mg/100 g BW, for 30 days), significantly increased hepatic enzymes in blood, sinusoidal congestion, disruption of central vein, inflammatory cell infiltration and hepatocellular necrosis in liver in dose dependent manner, with increase in NO, iNOS and ROS levels. In a kinetic study (single dose 227.5 mg/100 g BW), there was sequential decrease in GSH and enhanced NO suggesting free-radical generation as the primary cause of cell damage. It is concluded that the higher dosing of PTME or its continuous use for longer period (even in low doses) is hepatotoxicity by inducing oxidative stress.

摘要

野葛块根的甲醇提取物(豆科)(PTME)已在大鼠中进行了肝毒性测试。在急性研究中,PTME(100-400mg/100gBW,口服)的LD(50)为 227.5mg。对于亚慢性研究,其重复剂量(5-100mg/100gBW,30 天),以剂量依赖性方式显着增加血液中的肝酶、窦状隙充血、中央静脉中断、炎症细胞浸润和肝细胞坏死,同时增加 NO、iNOS 和 ROS 水平。在动力学研究(单次剂量 227.5mg/100gBW)中,GSH 依次减少,NO 增强,表明自由基生成是细胞损伤的主要原因。结论是,PTME 的较高剂量或其连续使用更长时间(即使在低剂量下)也会通过诱导氧化应激而导致肝毒性。

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