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首页> 外文期刊>Life sciences >Melatonin ameliorates carbon tetrachloride-induced hepatic fibrogenesis in rats via inhibition of oxidative stress
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Melatonin ameliorates carbon tetrachloride-induced hepatic fibrogenesis in rats via inhibition of oxidative stress

机译：褪黑素通过抑制氧化应激改善大鼠四氯化碳诱导的肝纤维化

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Melatonin is reported to exhibit a wide variety of biological effects, including antioxidant and anti-inflammatory. Evidence shows the important role of oxidative stress in the etiopathogenesis of hepatic fibrosis. The aim of this study was to investigate the protective effects of administration of melatonin in rats with carbon tetrachloride-induced fibrosis for 6 weeks. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examinations. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) levels were evaluated in tissue homogenates by spectrophotometry. The nuclear factor-kappaB (NF-kappa B) in liver tissue was examined by immunohistochemistry. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) concentrations in Kupffer cells (KCs) culture supernatants were measured with ELISA. The rats injected subcutaneously with CCl4 for 6 weeks resulted in hepatic fibrotic changes increased hydroxyproline and MDA levels, and decreased GSH-px and SOD levels, whereas melatonin reversed these effects. Furthermore, melatonin inhibited the expression of NF-kappa B in liver tissue and decreasing production of proinflammatory cytokines such as TNF-alpha and IL-1 beta from KCs in fibrotic rats. These present results suggest that melatonin ameliorates carbon tetrachloride-induced hepatic fibrogenesis in rats via inhibition of oxidative stress and proinflammatory cytokines production. (c) 2005 Elsevier Inc. All rights reserved.
机译：据报道，褪黑激素具有多种生物学作用，包括抗氧化剂和抗炎药。有证据表明氧化应激在肝纤维化的病因中起着重要的作用。这项研究的目的是研究褪黑激素对四氯化碳诱导的纤维化大鼠的保护作用，持续6周。通过测量组织羟脯氨酸水平和组织病理学检查对生化肝纤维化变化进行评估。脂质过氧化的最终产物丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH-px）和超氧化物歧化酶（SOD）的水平通过分光光度法在组织匀浆中评估。通过免疫组织化学检查肝组织中的核因子-κB（NF-κB）。用ELISA测量库普弗细胞（KCs）培养上清液中的肿瘤坏死因子-α（TNF-α）和白介素-1β（IL-1β）的浓度。皮下注射CCl4 6周的大鼠导致肝纤维化改变，羟脯氨酸和MDA水平升高，GSH-px和SOD水平降低，而褪黑激素逆转了这些作用。此外，褪黑素抑制了肝组织中NF-κB的表达，并降低了纤维化大鼠KCs促炎细胞因子如TNF-α和IL-1β的产生。这些目前的结果表明褪黑激素通过抑制氧化应激和促炎细胞因子的产生来改善大鼠的四氯化碳诱导的肝纤维化。 （c）2005 Elsevier Inc.保留所有权利。

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