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小球藻提取物可改善四氯化碳诱导的小鼠急性肝损伤。

Chlorella vulgaris extract ameliorates carbon tetrachloride-induced acute hepatic injury in mice.

作者信息

Li Li, Li Wei, Kim Yong-Ho, Lee Yong Woo

机构信息

Department of Smart Food and Drug, Graduate School, Inje University, 607, Obang-dong, 621-749 Gimhea, Gyeongman, South Korea.

出版信息

Exp Toxicol Pathol. 2013 Jan;65(1-2):73-80. doi: 10.1016/j.etp.2011.06.003. Epub 2011 Jul 8.

DOI:10.1016/j.etp.2011.06.003
PMID:21741806
Abstract

The possible protective effects of Chlorella vulgaris extract (CVE) on carbon tetrachloride (CCl(4))-induced acute hepatic injury in mice and the mechanism underlying these effects was investigated. CCl(4) administration caused a marked increase in the levels of serum aminotransferases, lipid peroxidation and cytochrome P450-2E1 (CYP450) expression. Also, decreased glutathione (GSH) content and activities of cellular antioxidant defense enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase and glutathione-S-transferase (GST) were found after CCl(4) exposure. All of these phenotypes were markedly reversed by preadministration of the mice with CVE. In addition, CVE exhibited antioxidant effects on FeCl(2)-ascorbate induced lipid peroxidation in mouse liver homogenates, and on superoxide radical scavenging activity. Taken together, these results suggest that CVE produced a protective action on CCl(4)-induced acute hepatic injury in mice, presumably through blocking CYP-mediated CCl(4) bioactivation, inducing the GSH levels, antioxidant enzyme activities and free radical scavenging effect. Therefore, CVE may be an effective hepatoprotective agent and viable candidate for treating hepatic disorders and other oxidative stress-related diseases.

摘要

研究了小球藻提取物(CVE)对四氯化碳(CCl₄)诱导的小鼠急性肝损伤的可能保护作用及其作用机制。给予CCl₄导致血清转氨酶水平、脂质过氧化和细胞色素P450 - 2E1(CYP450)表达显著增加。此外,在CCl₄暴露后,发现谷胱甘肽(GSH)含量降低,以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH - Px)、过氧化氢酶和谷胱甘肽 - S - 转移酶(GST)等细胞抗氧化防御酶的活性降低。预先给小鼠施用CVE可使所有这些表型显著逆转。此外,CVE对FeCl₂ - 抗坏血酸诱导的小鼠肝匀浆脂质过氧化以及超氧自由基清除活性具有抗氧化作用。综上所述,这些结果表明CVE对CCl₄诱导的小鼠急性肝损伤具有保护作用,可能是通过阻断CYP介导的CCl₄生物活化、诱导GSH水平、抗氧化酶活性和自由基清除作用。因此,CVE可能是一种有效的肝保护剂,是治疗肝脏疾病和其他氧化应激相关疾病的可行候选药物。

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