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Y-40138, a multiple cytokine production modulator, protects against D-galactosamine and lipopolysaccharide-induced hepatitis

机译：Y-40138是一种多种细胞因子产生调节剂，可预防D-半乳糖胺和脂多糖诱导的肝炎

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Acute and fulminant liver failure induced by viral hepatitis, alcohol or other hepatotoxic drugs are associated with tumor necrosis factor (TNF) production. D-Galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure. In this model, TNF-alpha plays a central role in the pathogenesis of D-GalN/LPS-induced liver injury in mice. Y-40138, N-[1-(4-[4-(pyrimidin-2-yl) piperazin-1-yl]methyl phenyl)cyclopropyl] acetamide HCl inhibits TNF-alpha and augments interleukin (IL)-10 production in LPS-injected mice in plasma. In the present study, we examined the effect of Y-40138 on D-GalN/LPS-induced hepatitis. Y-40138 (10mg/kg, i.v.) significantly suppressed TNF-alpha and monocyte chemoattractant protein-1 (MCP-1) production and augmented IL-10 production in plasma. In addition, Y-40138 significantly inhibited TNF-alpha production induced by direct interaction between human T lymphocytes and macrophages. Y-40138 suppressed plasma alanine transaminase (ALT) elevation and improved survival rate in D-GalN/LPS-injected mice, and it is suggested that the protective effect of Y-40138 on hepatitis may be mediated by inhibition of TNF-alpha and MCP-1, and/or augmentation of IL-10. This compound is expected to be a new candidate for treatment of cytokine and/or chemokine-related liver diseases such as alcoholic hepatitis. (c) 2006 Elsevier Inc. All rights reserved.
机译：由病毒性肝炎，酒精或其他肝毒性药物引起的急性和暴发性肝衰竭与肿瘤坏死因子（TNF）的产生有关。 D-半乳糖胺（D-GalN）和脂多糖（LPS）诱导的肝损伤是暴发性肝衰竭的实验模型。在该模型中，TNF-α在D-GalN / LPS诱导的小鼠肝损伤的发病机理中起着核心作用。 Y-40138，N- [1-（1- [4- [4-（嘧啶-2-基）哌嗪-1-基]甲基苯基）环丙基]乙酰胺HCl抑制LPS并增加LPS中白介素（IL）-10的产生血浆中注射小鼠。在本研究中，我们检查了Y-40138对D-GalN / LPS诱导的肝炎的作用。 Y-40138（10mg / kg，i.v.）显着抑制了血浆中TNF-α和单核细胞趋化蛋白1（MCP-1）的产生并增加了IL-10的产生。另外，Y-40138显着抑制人T淋巴细胞和巨噬细胞之间直接相互作用诱导的TNF-α产生。 Y-40138抑制了注射D-GalN / LPS的小鼠血浆丙氨酸转氨酶（ALT）升高，并提高了存活率，这表明Y-40138对肝炎的保护作用可能是通过抑制TNF-α和MCP介导的-1和/或IL-10增加。该化合物有望成为治疗细胞因子和/或趋化因子相关的肝脏疾病（例如酒精性肝炎）的新候选药物。 （c）2006 Elsevier Inc.保留所有权利。

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