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首页> 外文期刊>Life sciences >Secoisolariciresinol and isotaxiresinol inhibit tumor necrosis factor-alpha-dependent hepatic apoptosis in mice
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Secoisolariciresinol and isotaxiresinol inhibit tumor necrosis factor-alpha-dependent hepatic apoptosis in mice

机译：异豆香脂树脂和异麦角酚抑制小鼠肿瘤坏死因子-α依赖性肝细胞凋亡

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The effects of secoisolariciresinol (1) and isotaxiresinol (2), two major lignans isolated from the wood of Taxus yunnanensis, on tumor necrosis factor-alpha (TNF-alpha)-dependent hepatic apoptosis induced by D-galactosamine (D-GalN)/lipopolysaccharide (LPS) were investigated in mice. Co-administration Of D-GaIN (700 mg/kg) and LPS (10 mug/kg) resulted in a typical hepatic apoptosis characterized by DNA fragmentation and the formation of apoptotic bodies. Serum glutamic pyruvic transaminase (sGPT) and glutamic oxaloacetic transaminase (sGOT) levels were also raised at 8 h after D-GalN/LPS intoxication due to a severe necrosis of hepatocytes. Pre-administration of 1 or 2 (50, 10 mg/kg, i.p.) 12 and 1 h before D-GalN/LPS significantly reduced DNA fragmentation and prevented chromatin condensation, apoptotic body formation and hepatitis. Pro-inflammatory cytokines such as TNF-alpha and interferon-gamma (IFN-gamma) secreted from LPS-activated macropliages are important mediators of hepatocyte apoptosis in this model. Pre-treatment with 1 or 2 significantly inhibited the elevation of serum TNF-alpha and IFN-gamma levels. In a separate experiment, both lignans had a significant dose-dependent protective effect on D-GalN/TNF-alpha-induced cell death in primary cultured mouse hepatocytes and TNF-alpha-mediated cell death in murine L929 fibrosarcoma cells. These results indicated that 1 and 2 prevent D-GalN/LPS-induced hepatic injury by inhibiting hepatocyte apoptosis through the blocking of TNF-alpha and IFN-gamma production by activated macrophages and direct inhibition of the apoptosis induced by TNF-alpha. (C) 2004 Elsevier Inc. All rights reserved. [References: 35]
机译：从云南红豆杉的木材中分离出的两种主要木脂素癸二异豆香脂醇（1）和异麦角酚（2）对D-半乳糖胺（D-GalN）/诱导的肿瘤坏死因子-α（TNF-alpha）依赖性肝细胞凋亡的影响在小鼠中研究了脂多糖（LPS）。 D-GaIN（700 mg / kg）和LPS（10 mug / kg）的共同给药导致典型的肝细胞凋亡，其特征在于DNA片段化和凋亡小体的形成。 D-GalN / LPS中毒后，由于肝细胞严重坏死，血清谷氨酸丙酮酸转氨酶（sGPT）和谷草草酰乙酸转氨酶（sGOT）水平也升高。在D-GalN / LPS之前12和1小时预先给药1或2（50，10 mg / kg，i.p.）可显着减少DNA片段并防止染色质凝结，凋亡小体形成和肝炎。 LPS激活的巨噬细胞分泌的促炎细胞因子，例如TNF-α和干扰素-γ（IFN-γ）是该模型中肝细胞凋亡的重要介质。用1或2进行预处理可显着抑制血清TNF-α和IFN-γ的升高。在一个单独的实验中，两种木脂素对原代培养的小鼠肝细胞中D-GalN /TNF-α诱导的细胞死亡和鼠L929纤维肉瘤细胞中TNF-α介导的细胞死亡具有显着的剂量依赖性保护作用。这些结果表明1和2通过激活的巨噬细胞阻断TNF-α和IFN-γ的产生并直接抑制由TNF-α诱导的凋亡，从而抑制肝细胞凋亡，从而阻止了D-GalN / LPS诱导的肝损伤。 （C）2004 Elsevier Inc.保留所有权利。 [参考：35]

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