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目的:探讨尾加压素Ⅱ (urotensinⅡ, UⅡ) 受体拮抗剂urantide对急性肝衰竭 (acute liver failure, ALF) 小鼠肝组织p120-catenin (p120ctn) 表达的影响.方法:24只雄性Balb/c小鼠随机分为健康对照组、预处理对照组、ALF模型组和预处理ALF组 (6只/组) .ALF模型组和预处理ALF组均以脂多糖 (lipopolysaccharide, LPS) 50μg/kg联合D-半乳糖胺 (D-galactosamin, D-GalN) 800 mg/kg腹腔注射诱导ALF, 健康对照组注射等体积的0.9％氯化钠溶液;预处理ALF组在造模前30 min给予0.6 mg/kg urantide尾静脉注射;预处理对照组经同样预处理后腹腔注射等体积的0.9％氯化钠溶液.造模12 h后, 采集动物肝组织标本.肝组织p120ctn mRNA和蛋白质表达分别采用实时荧光定量PCR (real-time PCR) 和免疫印迹 (Western blot) 分析方法检测.结果:p120ctn mRNA和蛋白相对表达水平在健康对照组和预处理对照组之间差异无统计学意义;而健康对照组、预处理对照组和预处理ALF组p120ctn mRNA和蛋白相对表达水平均显著高于ALF模型组 (P ＜0.05) .结论:LPS/D-GalN诱导ALF小鼠肝内p120ctn表达受抑可能与UⅡ/UT信号系统的激活有关.“,”Objective:To investigate the effect of urantide, a urotensin Ⅱ receptor antagonist, on hepatic p120-catenin (p120 ctn expression in acute liver failure (ALF) mice. Methods:A total of 24 male Balb/c mice were randomly divided into the healthy control group, pretreatment control group, ALF model group and pretreatment ALF group (6/group). ALF model mice were induced by lipopolysaccharide (LPS) 50 μg/kg combined with D-galactosamine (D-GalN) 800 mg/kg intraperitoneal injection of ALF, and control mice were injected with an equal volume of 0.9％ sodium chloride solution;the pretreated ALF group was given a 0.6 mg/kg urantide tail vein injection 30 min before modeling;the pretreatment control group was replaced with an equal volume of 0.9％ sodium chloride solution. And then, liver specimens were collected after 12 h. The levels of hepatic p120 ctn mRNA and protein were detected by real-time PCR and Western blot analysis. Results:There was no significant difference in the relative expression levels of p120 ctn mRNA and protein between the healthy control group and the pretreatment control group, while the relative expression level of p120 ctn mRNA and protein in the healthy control group and the pretreatment ALF group was significantly higher than that in the ALF model group (P ＜0.05). Conclusion:The inhibition of p120 ctn expression may be associated with the activation of UⅡ/UT signaling system in LPS/D-GalN-induced ALF mice.