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丹酚酸A对四氯化碳诱导的大鼠急性肝损伤的保护作用。

Protective effect of salvianic acid a on acute liver injury induced by carbon tetrachloride in rats.

作者信息

Wang Chao-Yun, Ma Fu-Lu, Liu Jun-Tian, Tian Jing-Wei, Fu Feng-Hua

机构信息

Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Shaanxi, PR China.

出版信息

Biol Pharm Bull. 2007 Jan;30(1):44-7. doi: 10.1248/bpb.30.44.

Abstract

Previous research has shown that salvianic acid A [2-(3,4-dihydroxyphenyl)-2-hydroxy-propanoic acid, SA] extracted from Salvia miltiorrhiza BGE (Danshen) markedly inhibits lipid peroxidation of mitochondrial membrane of hepatic cells in vitro. The present study was conducted to examine protective effect of SA on liver injury induced by carbon tetrachloride (CCl4) and its possible mechanism in vivo. Male Sprague-Dawley rats weighing 180-200 g were used in the experiments. Five mmol/kg CCl4 in olive oil was given to rats i.p. Spectrophotometrical method was used to measure activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum, activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) as well as malondialdehyde (MDA) level in hepatic tissue and the rate of superoxide anion (O2*-) generation in hepatic submitochondrial particles. Hepatic histological structure was observed under light microscopy. CCl4 caused significant changes of activities of the enzymes, MDA level, and the rate of O2*- generation and histopathological changes of acute hepatic injury were noted. SA reversed the significant changes induced by CCl4. These results demonstrate that SA produces protective action on acute hepatic injury induced by CCl4 via an antioxidative mechanism.

摘要

先前的研究表明,从丹参中提取的丹酚酸A [2-(3,4-二羟基苯基)-2-羟基丙酸,SA] 在体外能显著抑制肝细胞线粒体膜的脂质过氧化。本研究旨在探讨SA对四氯化碳(CCl4)诱导的肝损伤的保护作用及其在体内的可能机制。实验采用体重180 - 200 g的雄性Sprague-Dawley大鼠。将5 mmol/kg CCl4溶于橄榄油中经腹腔注射给予大鼠。采用分光光度法测定血清中天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)的活性、肝组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性以及丙二醛(MDA)水平,以及肝亚线粒体颗粒中超氧阴离子(O2*-)的生成速率。在光学显微镜下观察肝脏组织学结构。CCl4引起了酶活性、MDA水平和O2*-生成速率的显著变化,并观察到急性肝损伤的组织病理学变化。SA逆转了CCl4诱导的显著变化。这些结果表明,SA通过抗氧化机制对CCl4诱导的急性肝损伤产生保护作用。

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