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首页> 外文期刊>Journal of natural products >Protective effects of hyperoside against carbon tetrachloride-induced liver damage in mice.
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Protective effects of hyperoside against carbon tetrachloride-induced liver damage in mice.

机译:金丝桃苷对四氯化碳诱导的小鼠肝损伤的保护作用。

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In this study, the hepatoprotective effects of hyperoside (1), a flavonoid glycoside isolated from Artemisia capillaris, have been examined against carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with vehicle or 1 (50, 100, and 200 mg.kg-1) 30 min before and 2 h after CCl4 (20 micro L.kg-1) injection. Levels of serum aminotransferases were increased 24 h after CCl4 injection, and these increases were attenuated by 1. Histological analysis showed that 1 prevented portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia. Lipid peroxidation was increased and hepatic glutathione content was decreased significantly after CCl4 treatment, and these changes were reduced by administration of 1. Protein and mRNA expression of tumor necrosis factor- alpha (TNF- alpha ), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) and nuclear protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) significantly increased after CCl4 injection. Compound 1 suppressed TNF- alpha , iNOS, and COX-2 protein and mRNA expression and augmented HO-1 protein and mRNA expression and Nrf2 nuclear protein expression. These results suggest that 1 has protective effects against CCl4-induced acute liver injury, and this protection is likely due to enhancement of the antioxidative defense system and suppression of the inflammatory response.
机译:在这项研究中,已研究了从o蒿(Artemisia capillaris)分离出的黄酮苷Hyperoside(1)对四氯化碳(CCl 4 )诱导的肝损伤的肝保护作用。在CCl 4 (20 micro L.kg)之前和之后30分钟,用溶媒或1(50、100和200 mg.kg -1 )腹膜内处理小鼠。 -1 )注入。注射CCl 4 后24小时,血清氨基转移酶的水平增加,而这些增加被1减弱。组织学分析显示1预防了门脉炎症,中心性坏死和库普弗细胞增生。 CCl 4 处理后脂质过氧化增加,肝谷胱甘肽含量显着降低,并且通过施用1可以减少这些变化。肿瘤坏死因子-α(TNF-α)的蛋白和mRNA表达CCl 4后,一氧化氮合酶(iNOS),环加氧酶-2(COX-2)和血红素加氧酶-1(HO-1)以及核因子红系2相关因子2(Nrf2)的核蛋白表达显着增加。 注入。化合物1抑制TNF-α,iNOS和COX-2蛋白和mRNA表达,并增加HO-1蛋白和mRNA表达以及Nrf2核蛋白表达。这些结果表明1具有抗CCl 4 诱导的急性肝损伤的作用,并且这种保护作用可能是由于增强了抗氧化防御系统和抑制了炎症反应。

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