Adiponectin deficiency exacerbates lipopolysaccharide/D-galactosamine-induced liver injury in mice
Adiponectin deficiency exacerbates lipopolysaccharide/D-galactosamine-induced liver injury in mice
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DOI：
10.3748/wjg.v12.i21.3352
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发表时间：
2006-06-07
影响因子：
4.3
通讯作者：
Hayashi, Norio
中科院分区：
文献类型：
--
作者：
Matsumoto, Hitoshi;Tamura, Shinji;Hayashi, Norio
目的：目的：探讨脂联素（adiponectin）对脂多糖（lipopolysaccharide，LPS）诱导的肝损伤的关键调节因子枯否细胞（Kupffer cell）功能的影响。结果：与野生型小鼠相比，GalN/LPS基因敲除小鼠的存活率显著降低，血浆丙氨酸转氨酶和肿瘤坏死因子-α（TNF-α）水平显著升高，IL-10水平显著降低。与野生型小鼠相比，基因敲除小鼠肝脏中TNF-α基因的表达更高，而IL-10基因的表达更低。在培养的脂联素预处理库普弗细胞，脂多糖显着降低TNF-α的水平和提高IL-10，在培养基中的水平和各自的基因表达水平，与库普弗细胞相比，没有adiponectin预treatment.CONCLUSION：脂联素抑制TNF-α的生产，并诱导IL-10的生产库普弗细胞在响应LPS刺激，和缺乏脂联素增强I脂多糖诱导的肝损伤。(C)2006年，WJG出版社。All rights reserved.
AIM: To examine the effects of adiponectin on the functions of Kupffer cells, key modulators of lipopolysaccharide (LPS)-induced liver injury.METHODS: D-galactosamine (GalN) and LPS were injected intraperitoneally into adiponectin-/- mice and wild type mice. Kupffer cells, isolated from Sprague-Dawley rats, were preincubated with or without adiponectin, and then treated with LPS.RESULTS: In knockout mice, GalN/LPS injection significantly lowered the survival rate, significantly raised the plasma levels of alanine transaminase and tumor necrosis factor-alpha (TNF-alpha) and significantly reduced IL-10 levels compared with wild type mice. TNF-alpha gene expression in the liver was which higher and those of IL-10 were lower in knockout mice than in wild type mice. In cultured adiponectin-pre-treated Kupffer cells, LPS significantly lowered TNF-alpha levels and raised IL-10,levels in the culture media and their respective gene expression levels, compared with Kupffer cells without adiponectin-pre-treatment.CONCLUSION: Adiponectin supresses TNF-alpha production and induces IL-10 production by Kupffer cells in response to LPS stimulation, and a lack of adiponectin enhances I LPS-induced liver injury. (C) 2006 The WJG Press. All rights reserved.