Adiponectin deficiency exacerbates lipopolysaccharide/ D-galactosamine-induced liver injury in mice
Adiponectin deficiency exacerbates lipopolysaccharide/ D-galactosamine-induced liver injury in mice作者机构:Department of Gastroenterology and Hepatology Osaka UniversityGraduate School of Medicine2-2K1Yamada-okaSuitaOsaka 565-0871Japan Department of Metabolic Medicine Osaka UniversityGraduate School of Medicine2-2B5Yamada-okaSuitaOsaka 565-0871Japan Sumitomo Hospital 5-3-20Kita-Ku nakanoshimaOsaka530-0005Japan
出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))
年 卷 期:2006年第12卷第21期
页 面:3352-3358页
核心收录:
学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
主 题:Adiponectin Lipopolysaccharide Kupffer cell TNF-alpha IL10
摘 要:AIM: To examine the effects of adiponectin on the functions of Kupffer cells, key modulators of lipopolysaccharide (LPS) -induced liver ***: D-galactosamine (GAIN) 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 ***: In knockout mice, GalN/LPS injection significantly lowered the survival rate, significantly raised the plasma levels of alanine transaminase and tumor necrosis factor-α (TNF-α) and significantly reduced IL-10 levels compared with wild type mice. TNF-α 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-α levels and raised IL-10 levels in the culture media and their respective gene expression levels, compared with Kupffer cells without ***: Adiponectin supresses TNF-α production and induces IL-10 production by Kupffer cells in response to LPS stimulation, and a lack of adiponectin enhances LPS-induced liver injury.