The effect of chondroitin sulfate against CCl4-induced hepatotoxicity.
The effect of chondroitin sulfate against CCl4-induced hepatotoxicity.
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DOI：
10.1248/bpb.26.622
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发表时间：
2003-05
影响因子：
2
通讯作者：
Bae-jin Ha;Jin Young Lee
中科院分区：
文献类型：
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作者：
Bae-jin Ha;Jin Young Lee
本研究旨在开发一种用于抗氧化药物的新型生物材料。在这项研究中，硫酸软骨素（CS）（100 mg/kg和200 mg/kg体重）的肝保护作用进行了研究，在肝总匀浆和线粒体组分的抗氧化酶水平。采用四氯化碳（CCl（4））诱导的大鼠肝损伤模型。CCl（4）诱导的大鼠肝毒性模型因其实用、简便、经济等优点而被广泛应用，因为CCl（4）注射产生的自由基是引起肝毒性的重要因素。测定肝组织丙二醛（MDA）含量、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、还原型谷胱甘肽（GSH）、氧化型谷胱甘肽（GSSG）和谷胱甘肽过氧化物酶（GPx）活性。此外，还对肝组织进行了组织病理学研究。肝抗氧化酶活性升高，而MDA浓度降低，在所有CS治疗的动物。结果表明，CS以剂量依赖性方式保护氧化应激。CS治疗组肝组织炎症反应和肝硬化程度明显减轻。它给我们的印象是CS可能是一个激进的清道夫。
This study was conducted to develop a new biomaterial to be used for an antioxidative drug. In this study, the hepatoprotective effect of chondroitin sulfate (CS) (100 mg/kg and 200 mg/kg body weight) was investigated at the antioxidative enzyme levels of liver total homogenate and mitochondria fraction. And the carbone tetrachloride (CCl(4))-induced rats were used as hepatotoxic models. The CCl(4) induced rat has been widely used as a hepatotoxic model due to its practicality, convenience and cost effectiveness since the generation of free oxygen radicals by CCl(4) injection was proposed as an important causative agent of hepatotoxicity. Malondialdehyde (MDA) levels were determined as well as the activities of superoxide dismutase (SOD), catalase (CAT), reduced-glutathione (GSH), oxidized-glutathione (GSSG) and glutathione peroxidase (GPx) in the liver. In addition, histopathology of liver tissue was investigated. Liver antioxidative enzyme activity was elevated while MDA concentration was decreased in all CS treated animals. The results demonstrated that CS protected oxidative stress in a dose dependent manner. Moreover, inflammation and cirrhosis in liver tissue of CS treated group were significantly decreased. It gave us an impression that CS might be a radical scavenger.